{"title":"Erythrocyte sodium-lithium countertransport in Chinese: its relationship to family history of hypertension.","authors":"Y T Lau, D Wu, H C Liang, M C Chen","doi":"10.3109/10641969209036202","DOIUrl":"https://doi.org/10.3109/10641969209036202","url":null,"abstract":"<p><p>Rates of sodium (Na+)-stimulated lithium (Li+) efflux (Na(+)-Li+ countertransport) and ouabain-sensitive Na+ efflux (Na+ pump) were determined in erythrocytes of Chinese normotensive and hypertensive subjects. Near-maximal rate of Na(+)-Li+ countertransport was found to be significantly higher in hypertensive than normotensive subjects. No significant difference was observed for the rate of Na+ pump between them. A second series of study involved normotensive subjects without and with hypertensive parent(s) (group A and B, respectively) and hypertensive subjects (group C). We found that the rate of Na(+)-Li+ countertransport in group A was significantly lower than that of group B and C, while no difference existed between group B and C. No significant difference was observed for the rate of Na+ pump among the three groups. Our results suggested that Na(+)-Li+ countertransport activity could be a genetic marker for essential hypertension in Chinese, similar to that as proposed in Caucasians.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 3","pages":"489-503"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036202","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12491792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"ACTH hypertension in the rat: role of sodium chloride.","authors":"M Li, J A Whitworth","doi":"10.3109/10641969209036208","DOIUrl":"https://doi.org/10.3109/10641969209036208","url":null,"abstract":"<p><p>Adrenocorticotrophin (ACTH) produces adrenally dependent increases in both blood pressure and salt (NaCl) appetite in the rat. The present study examines the effect of free access to a high intake of NaCl on ACTH hypertension in the rat to test the hypothesis that high NaCl intake would amplify the rise in blood pressure. Either water or 1%NaCl were offered to sham or ACTH treated Sprague-Dawley rats. Subcutaneous injections of synthetic ACTH (0.5 mg/kg/day) for 10 days caused large increases in the intake of both 1%NaCl (+240 +/- 6 ml/day) and water (+45 +/- 4 ml/day), urine volume (1%NaCl + ACTH +182 +/- 4 ml/day, ACTH + water +36 +/- 2 ml/day), adrenal weight (ACTH + water 176 +/- 18, ACTH + 1%NaCl 367 +/- 129 mg/100 g body weight) and maximum systolic blood pressure (SBP) (ACTH + water +18 +/- 5 mmHg; 1%NaCl + ACTH +16 +/- 3 mmHg). Some ACTH + 1%NaCl rats developed severe edema. Thus, free access to NaCl in ACTH treated Sprague Dawley rats did not potentiate the hypertension, but was associated with edema in some animals.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 4","pages":"567-85"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036208","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12495303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Protein kinase C and cell proliferation in spontaneously hypertensive rats.","authors":"D L Zhu, T Herembert, P Marche","doi":"10.3109/10641969209036224","DOIUrl":"https://doi.org/10.3109/10641969209036224","url":null,"abstract":"<p><p>Cultured aortic fibroblasts from spontaneously hypertensive rats (SHR) exhibit increased proliferation rate compared with cells from normotensive Wistar Kyoto (WKY) rats. The present study was designed to investigate whether this growth abnormality could be accounted for by alteration in protein kinase C (PKC). The enzyme activation by 12-O-tetradecanoyl phorbol 13-acetate (TPA) promoted 3H-thymidine incorporation which was higher in SHR-derived fibroblasts compared with WKY-derived cells. Likewise, 3H-phorbol 12,13-dibutyrate (PDBu) binding to intact cells was markedly increased in SHR-derived fibroblasts. These findings suggest a difference in PKC activity between the two cell types. In both cell types, serum-induced 3H-thymidine incorporation was enhanced by PKC down-regulation, which was obtained by prolonged treatment of cells with high dose of TPA, whereas it was inhibited in a dose-dependent manner by activation of the enzyme. The changes in serum-induced 3H-thymidine incorporation elicited either by activation or desensitization of PKC, did not differ between SHR and WKY fibroblasts. Our results indicate therefore i) that in the presence of serum PKC exerts an antiproliferative effect in rat aortic fibroblasts and ii) that the increase in PKC activity and in sensitivity to TPA exhibited by SHR-derived fibroblasts, is not involved in the increased proliferation rate displayed by SHR-derived fibroblasts in serum-containing medium.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 5","pages":"875-87"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12565815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
F Veglio, G Pinna, R Melchio, F Rabbia, M Panarelli, D Schiavone, P Mulatero, L Chiandussi
{"title":"Hormonal aspects of the relation of liver cirrhosis to essential hypertension.","authors":"F Veglio, G Pinna, R Melchio, F Rabbia, M Panarelli, D Schiavone, P Mulatero, L Chiandussi","doi":"10.3109/10641969209036225","DOIUrl":"https://doi.org/10.3109/10641969209036225","url":null,"abstract":"<p><p>The association of liver cirrhosis with arterial essential hypertension has been previously described. The present study extends the previous reports by investigating the hormonal relationships that may occur in patients with established essential hypertension associated to liver cirrhosis. We studied the renin-angiotensin, the adrenergic systems and other vasoactive hormones such as arginine-vasopressin, atrial natriuretic peptide, endothelin and parathyroid hormone in cirrhotic patients with and without essential hypertension. The data suggested that the coincidence of arterial hypertension in cirrhotic patients was characterized by the following findings: a decreased renin-angiotensin activity; a reduced systemic vasodilatation; an increased peripheral pressor effect of vasoactive hormones and an increased effective blood volume.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 5","pages":"889-903"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036225","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12565816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M Peral de Bruno, A Coviello, M Meyer, W G Forssmann
{"title":"Relaxation of non-contracted smooth muscle by atrial natriuretic peptide.","authors":"M Peral de Bruno, A Coviello, M Meyer, W G Forssmann","doi":"10.3109/10641969209038197","DOIUrl":"https://doi.org/10.3109/10641969209038197","url":null,"abstract":"<p><p>Atrial natriuretic peptide (alpha-hANP-99-126), 1 x 10(-8) to 5 x 10(-10) M was able to further relax the non-contracted aortic smooth muscle of rabbit after complete recovery from a previous challenge with human angiotensin II (AII), 1 x 10(-6) M. The relaxation was directly proportional to the response of the ring or strip to the previous challenge with AII. ANP does not have effect on basal tension in isolated strips or rings of the rabbit aorta not previously exposed to AII. Norepinephrine (NE), 10(-7) M was less potent in inducing reactivity of the vessel to ANP, ie, only a small relaxant effect on basal tension could be observed. A similar vasorelaxant effect of ANP on basal tension could be obtained in the absence of extracellular calcium: Ca(2+)-free Ringers' solution containing 2 mM ethylene-glycol-bis (beta-aminoethyl ether)N',N' tetraacetic acid (EGTA-Ringer). In contrast, sodium nitroprusside 10(-8) M does not affect basal tension. Present results demonstrate the role of the physiological state of the vessel in the reactivity to ANP.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 6","pages":"1125-39"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209038197","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12596078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Factors associated with acute salt-sensitivity in borderline hypertensive patients.","authors":"C Borghi, S Boschi, F V Costa, E Ambrosioni","doi":"10.3109/10641969209036222","DOIUrl":"https://doi.org/10.3109/10641969209036222","url":null,"abstract":"<p><p>The acute sensitivity to sodium loading has been investigated in 26 borderline hypertensive patients (BHT) undergoing acute i.v. NaCl infusion. Measurements included blood pressure (BP), forearm vascular resistance (FVR) and venous distensibility (VV30), plasma renin activity (PRA), plasma aldosterone, plasma atrial natriuretic factor (ANF), and plasma levels of endogenous Na+/K+ATPase inhibitor. Sodium loading was associated with a greater than 8% increase in mean BP in 12 patients defined as salt-sensitive (NaCl-SENS) in comparison to salt-insensitive (NaCl-INSENS) subset. NaCl-SENS patients in comparison to NaCl-INSENS exhibited 1) a greater baseline VV30 (2.1 vs 1.4 ml/100 ml; p less than .005), and a response to saline characterized by 2) increased FVR (21.4 vs -6.5%; p less than .005), 3) blunted PRA suppression (-42 vs -67%; p less than .05), 4) delayed ANF response and 5) release of a Na+/K+ATPase inhibitor. Post-loading cumulative urinary sodium excretion was reduced in NaCl-SENS borderline hypertensives compared to NaCl-INSENS (2.6 vs 3.8 mumol/min/Kg; p less than .05). We conclude that acute salt-sensitivity in BHT is characterized by a blunted hormonal response to sodium loading which could be responsible of the activation of hemodynamic as well as humoral mechanisms leading to progressive blood pressure increase.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 5","pages":"837-51"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036222","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12567293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of immobilization stress on renal sympathetic neurotransmission.","authors":"D C Eikenburg","doi":"10.3109/10641969209036199","DOIUrl":"https://doi.org/10.3109/10641969209036199","url":null,"abstract":"<p><p>The effects immobilization stress on renal sympathetic neurotransmission as well as on heart, spleen and adrenal catecholamine content were examined in the rat. A single 2.5 hr stress period produced significant increases in blood pressure, heart rate, plasma norepinephrine and plasma epinephrine concentrations. However, no changes in renal catecholamine content or in stimulus-induced (1 Hz, 120 pulses, supramax. V) overflow of catecholamines were observed when the isolated perfused rat kidney was studied immediately after the 2.5 hr stress period. In contrast, the single stress period produced a 3-4 fold increase in cardiac epinephrine content while no effects on spleen or adrenal catecholamine content were observed. When stress was applied for 7 daily 2.5 hr periods, the repetition of the stress failed to produce any changes in renal neurotransmitter content or stimulus-induced overflow from the isolated perfused rat kidney. The data suggest that the accumulation of epinephrine into peripheral sympathetic nerves as a result of stress-induced adrenal catecholamine release is not a phenomenon which can be generalized to all regions of the cardiovascular system.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 3","pages":"435-51"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036199","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12492441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Renal renin secretion rate and norepinephrine secretion rate in response to centrally administered angiotensin-II: role of the medial basal forebrain.","authors":"L B Weekley","doi":"10.3109/10641969209036227","DOIUrl":"https://doi.org/10.3109/10641969209036227","url":null,"abstract":"<p><p>The influence that centrally administered angiotensin-II (ANG-II) and saralasin (SAR) has on renal norepinephrine secretion rate (NESR) and renal renin secretion rate (RSR) were studied. Rats were given thermal lesions of the medial basal forebrain (MBF) or sham surgery. Twenty-four hours later the right kidney was vascularly isolated (but neurally intact) and perfused with an artificial plasma at either a constant pressure (100 mm Hg) or constant flow (600 microliters/min). Renal perfusate was collected before (pre-injection) and at 10 min intervals after central administration of peptides for determination of NESR and RSR. In both perfusion models, intracerebroventricular (ICV) ANG-II increased renal NESR. In MBF lesioned rats pre-injection renal NESR is reduced and the response to ICV ANG-II is blocked. In both perfusion models ICV ANG-II decreases renal RSR. Concomitant administration of SAR blocks the effect of ANG-II on both NESR and RSR. MBF lesioned rats had significantly elevated pre-injection levels of RSR and there is no change in RSR following ICV ANG-II. These experiments indicate that centrally administered ANG-II increases renal NESR concomitant with a decrease in renal RSR and that MBF lesions block those changes.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 5","pages":"923-45"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036227","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12565818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R Karlsson, T Stigbrand, J Oscarsson, S Edén, J Bouhnik, M Celio, B von Schoultz
{"title":"Effects of growth hormone and estrogen on rat angiotensinogen quantified by an enzyme linked immunosorbent assay.","authors":"R Karlsson, T Stigbrand, J Oscarsson, S Edén, J Bouhnik, M Celio, B von Schoultz","doi":"10.3109/10641969209036206","DOIUrl":"https://doi.org/10.3109/10641969209036206","url":null,"abstract":"<p><p>An enzyme linked immunosorbent assay for rat angiotensinogen was developed based on one monoclonal antibody with high affinity for angiotensinogen and des-angiotensin 1-angiotensinogen and rabbit polyclonal antibodies for angiotensinogen was developed. Serum levels of angiotensinogen were lower in female than in male rats but increased significantly after hypophysectomy. Estrogen substitution after hypophysectomy had no further stimulatory or inhibitory influence. In hypophysectomized animals continuous and intermittent growth hormone administration had clearly different effects. The results indicate that the sexually dimorphic secretion of growth hormone is involved in the regulation of circulating angiotensinogen concentrations in the rat.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 3","pages":"551-63"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036206","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12767594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of gonadal hormones in hypertension in the Dahl salt-sensitive rat.","authors":"N E Rowland, M J Fregly","doi":"10.3109/10641969209036195","DOIUrl":"https://doi.org/10.3109/10641969209036195","url":null,"abstract":"<p><p>The present studies examine the effect of gonadal hormones on the development of hypertension in Dahl salt-sensitive rats fed a high salt diet. In the first study, administration of estradiol benzoate did not prevent hypertension in either adult ovariectomized females or intact males. In a second study, neonatal castration of males slowed the onset of salt-induced hypertension, and females that were treated neonatally with testosterone developed somewhat higher pressures that did untreated females. These data extend to Dahl S rats the findings observed originally in spontaneously hypertensive rats that blood pressure is modulated by gonadal hormones. These results are consistent with the conclusion that gonadal hormones may exert organizational effects on cardiovascular control regions of the brain during early postnatal development in rats.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 3","pages":"367-75"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036195","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12767733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}