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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of calcium supplementation on blood pressure, intracellular free calcium concentration ([Ca2+]i) and rate of Na(+)-H+ exchange were studied in DOC-NaCl-hypertensive rats. All the animals were uninephrectomized and divided into two main groups: the first group received deoxycorticosterone (DOC) (25 mg/kg, s.c.) once a week and had 0.7% NaCl as drinking fluid while the other received equal volumes of saline and tap water to drink. The animals were further divided according to dietary calcium intake: in the Control and DOC groups the chow contained 1.1% calcium, in the Calcium and DOC+Calcium groups, 2.5%. After 6 and 8 weeks, blood pressure in the DOC group was higher than in the Control group; on the other hand, the development of hypertension was attenuated in the DOC+Calcium compared with the DOC group. The Control and Calcium groups did not differ from each other. Platelets and lymphocytes were used as experimental models to study changes in the regulation of [Ca2+]i, evaluated by fluorescent indicators indo-1 and quin-2. In lymphocytes, basal [Ca2+]i was highest in the DOC group, but similar in DOC+Calcium and Control groups. In platelets, both basal and thrombin-stimulated [Ca2+]i were higher in the DOC and DOC+Calcium groups than in the Control group. In both cell types [Ca2+]i was similar in Control and Calcium groups. In addition, platelets were used to study the ability of the cells to recover from intracellular acidification by first blocking the Na(+)-H+ exchange in a Na(+)-free medium and then restarting the exchange mechanism by increasing the extracellular Na+ concentration at constant speed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of high calcium intake on intracellular free [Ca2+] and Na(+)-H+ exchange in DOC-NaCl-hypertensive rats. 144 51

Magnesium concentrations in erythrocyte ghosts and arterial tissue of male, spontaneously hypertensive rats (SHR) were significantly less than in these tissues of male normotensive controls (Wistar-Kyoto; WKY) of the same age, which were also fed rat chow and tap water. The magnesium concentration in SHR erythrocyte ghosts was increased to the control value by incubating SHR erythrocytes with WKY blood plasma; SHR plasma did not affect the magnesium concentration in WKY erythrocyte ghosts. The magnesium concentrations in erythrocyte ghosts, aortas, and mesenteric arteries from female salt-sensitive (SS/JR) and salt-resistant (SR/JR) Dahl-derived rats, both maintained ad libitum on laboratory rat chow and either tap water or 0.9% NaCl, were not different but were significantly less than those of Sprague-Dawley rats considered as controls. While the ingestion of 0.9% NaCl had no effect on the magnesium concentrations measured in these animals, it caused the salt-sensitive rats to become severely hypertensive. It is evident from these observations that the decreased binding of magnesium to the plasma membrane of cells may be an inheritable metabolic defect that may be associated with the development of hypertension. However, in those instances of hypertension in which this defect occurs, it appears to be a contributing cause of the hypertension; by itself the defect is not a cause of hypertension.
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PMID:Abnormal magnesium metabolism in two rat models of genetic hypertension. 149 90

This study examines the effects of a 6-week exposure to 1% NaCl in tap water with and without desoxycorticosterone acetate (DOCA) on renal alpha adrenoceptors and systolic blood pressure (SBP) in spontaneously hypertensive adult rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. On normal sodium intake, SHR had higher renal alpha 1- (p less than 0.05) and alpha 2-adrenoceptor densities (p less than 0.001) and SBP (p less than 0.001) than WKY rats. Although WKY rats given either 1% NaCl, DOCA, or DOCA plus 1% NaCl developed hypertension after 6 weeks of treatment, only 1% NaCl administration for the same period produced an increase in the alpha 1-adrenoceptor density when compared to the control (p less than 0.001). In SHR, ingestion of 1% NaCl or DOCA plus 1% NaCl increased the already elevated alpha 2-adrenoceptor density (p less than 0.001) and SBP even more in this strain after 6 weeks of treatment. Equilibrium dissociation constants (Kd), however, were similar for both classes of receptors in experimental and control rats. The results of this study indicate that only the combination of 1% NaCl in tap water and DOCA administration is effective in accelerating hypertension in adult SHR. On the other hand, in this form of genetic rat hypertension, exaggerated sodium intake with or without DOCA administration could presumably be correlated with the increased renal alpha 2 adrenoceptors observed in these animals.
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PMID:Altered renal alpha-adrenoceptor density induced by prolonged NaCl and DOCA administration in spontaneously hypertensive rats. 169 6

Effects of high salt intake on the early onset of hypertension were examined in two-kidney, one-clip rats. They were divided into high salt and control groups which were supplied with 1.0% NaCl and tap water, respectively, as a drinking solution for 12 days after clipping the left renal artery. The high salt group showed a lower plasma renin concentration and a higher plasma atrial natriuretic peptide (ANP) along with an attenuation of the magnitude of early hypertension, as compared with the control group. A significant positive correlation between blood pressure and plasma renin concentration and an inverse correlation between plasma renin concentration and ANP were shown. Cortical renal renin content was comparable between the two groups. In another two groups of sham-clipped rats, the high salt group did not differ from the tap water-drinking group in any of the parameters examined, except that ANP was significantly higher. These results demonstrate that high salt intake attenuates the developmental phase of hypertension in two-kidney, one-clip rats by increasing the ANP and suppressing the release of renin.
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PMID:High salt intake attenuates the development of hypertension in two-kidney, one-clip Goldblatt rats. 182 73

In previous studies we found that vasopressin stimulation of both cyclic AMP (cAMP) formation in cortical collecting tubules (CCT) and sodium reabsorption in isolated perfused kidneys was markedly exaggerated in rats with mineralocorticoid hypertension. In the present study, we tested the response (cAMP accumulation) of cortical and outer medullary collecting tubules (OMCT) to vasopressin in two rat models that are resistant to deoxycorticosterone acetate (DOCA)-induced hypertension, the Wistar-Furth strain and NaCl-deficient rats. The blood pressure of normal outbred Wistar rats rose to hypertensive levels (systolic pressure more than 165 mm Hg) during a 5-week treatment with DOCA (10 mg/week) and 1% saline to drink. Significant hypertrophy of the heart and kidneys was also observed. Vasopressin (10(-8) M)-induced cAMP formation was enhanced 3.4-fold in the CCT (OMCT unchanged) of hypertensive rats compared with normotensive controls. Significant hypertrophy (as indexed by tubule diameter) of the CCT but not the OMCT was also observed in DOCA-salt hypertensive rats. Restriction of dietary NaCl (0.13% in chow, tap water to drink) completely prevented DOCA-induced hypertension, organ and CCT hypertrophy, and enhancement of vasopressin-stimulated cAMP formation in the CCT. In Wistar-Furth rats, DOCA-salt treatment did not alter blood pressure or cause significant organ hypertrophy. However, DOCA-salt treatment enhanced vasopressin-stimulated cAMP formation by 4.1-fold in CCT of Wistar-Furth rats, with significant tubular hypertrophy in the CCT but not the OMCT. We conclude that DOCA-induced hypertension and changes in CCT function are dependent on excess dietary NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jan
PMID:Vasopressin response in collecting ducts of rats resistant to mineralocorticoid hypertension. 184 20

This study examined the effect of moderate ethanol intake on systolic blood pressure, platelet cytosolic free calcium, aortic calcium, and rubidium-86 uptake in Wistar-Kyoto rats. Twelve Wistar-Kyoto rats, aged 6 weeks, were given 5% ethanol in drinking water the first week followed by 10% ethanol in drinking water for the next 6 weeks. Twelve control animals were given regular tap water. Systolic blood pressure in the ethanol-treated rats was significantly higher (p less than 0.05) than that in controls after 1 week and remained higher throughout the study. At 13 weeks of age, platelet cytosolic free calcium and calcium uptake by aortas were significantly higher (p less than 0.001) in ethanol-treated animals as compared with those in controls. Ethanol intake did not affect aortic ouabain-sensitive 86Rb uptake. The in vitro effect of ethanol on calcium-45 and 86Rb uptake was also investigated in aortas of untreated Wistar-Kyoto rats at 13 weeks of age. In vitro ethanol (2.5-20 mmols/l) did not significantly affect 45Ca and 86Rb uptake in rat aortas. The increases in systolic blood pressure, platelet cytosolic free calcium, and vascular calcium uptake suggest that increases in cytosolic free calcium and calcium uptake mechanisms are associated with ethanol-induced hypertension.
Hypertension 1991 Jul
PMID:Platelet-free calcium and vascular calcium uptake in ethanol-induced hypertensive rats. 186 Jul 6

This study was performed to determine if an alteration in vascular polyamine contents is associated with the development of deoxycorticosterone acetate-salt hypertension. The effects of chronic administration of alpha-difluoromethylornithine, a specific irreversible inhibitor of ornithine decarboxylase and thus polyamine biosynthesis, on vascular polyamine contents, structure, and function as well as the development of hypertension was studied. Control and deoxycorticosterone acetate-salt rats received either tap water or a drinking solution containing alpha-difluoromethylornithine for 6 weeks, during which period systolic blood pressures were recorded. Vascular reactivity studies were performed on rings of aorta and tail artery. Medial thickness, vessel weight, and vascular polyamine contents were also assessed in these arteries. alpha-difluoromethylornithine treatment had no significant effect on either systolic blood pressure or vascular structure, function, and polyamine contents of control animals. The elevation in blood pressure and the increase in medial thickness, ring weight, and vascular polyamine contents as well as altered vascular reactivity observed in deoxycorticosterone acetate-salt rats was significantly attenuated by alpha-difluoromethylornithine treatment. These results are the first to demonstrate that vascular polyamine contents are elevated in the deoxycorticosterone acetate-salt rat and that chronic alpha-difluoromethylornithine treatment prevents the rise in vascular polyamines as well as the elevation in blood pressure and attendant changes in the vasculature. Thus, the increase in vascular polyamines may comprise a critical link between the initiating stimuli and the alterations in vascular structure and function implicated in the pathogenesis of deoxycorticosterone acetate-salt hypertension.
Hypertension 1991 Jul
PMID:Polyamines, vascular smooth muscle, and deoxycorticosterone acetate-salt hypertension. 186 Jul 16

Male Sprague-Dawley rats were uninephrectomized and given either deoxycorticosterone (DOC) pivalate (12.5 mg three times weekly) and 1% NaCl/0.2% KCl to drink for 4 weeks (DOC-treated), after which DOC was stopped and tap water substituted (post-DOC), or tap water to drink throughout (controls), DOC treatment increased blood pressure, serum sodium, plasma atrial natriuretic peptide (P-ANP) and plasma deoxycorticosterone (P-DOC) (P less than 0.05), while serum potassium, plasma renin and plasma angiotensin II were lower (P less than 0.05) than in control animals. Plasma vasopressin (P-AVP) was also raised but not significantly. These changes persisted for up to 4 weeks post-DOC and, in the case of plasma renin, plasma angiotensin II, P-AVP and P-ANP, for up to 12 weeks. Total body sodium was also increased at 2 weeks post-DOC (P less than 0.05). Rats which were adrenalectomized after 4 weeks of DOC treatment in which DOC injections were stopped, then drank either NaCl/KCl or tap water; blood pressure and P-DOC remained elevated while plasma renin remained suppressed. There were more deaths in rats given NaCl/KCl (five of six) than in the group given water (one of six). Rats treated with a subcutaneous DOC silastic implant had a comparable rise in blood pressure to rats given DOC injections. However, after removal of the implant, while blood pressure remained elevated, P-DOC levels were not raised and plasma renin rose to control levels after 4 weeks. These findings indicate that, in rats given DOC injections, post-DOC hypertension results from sodium and fluid retention as a consequence of chronic hangover of exogenously administered DOC.
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PMID:Hormone and electrolyte changes in post-deoxycorticosterone salt hypertension in rats. 196 84

Hyperuricemia is present in 20-40% of pediatric and adult patients with essential hypertension. This metabolic abnormality may represent an additional risk factor for the development of cardiovascular disease. Therefore, we performed the following studies to determine 1) whether hyperuricemia is more prevalent in the spontaneously hypertensive rat (SHR) and 2) whether allopurinol treatment has a beneficial effect on the development of hypertension in this strain, based on its capacity to lower the serum uric acid concentration and to act as an antioxidant agent. SHR and control Wistar-Kyoto (WKY) rats were assigned to two groups, one given tap water to drink and the other provided water containing allopurinol (400 mg/l) to furnish an approximate daily dose equal to 100 mg/kg body wt. This treatment was maintained for 15 weeks. The serum uric acid levels were similar in untreated SHR and WKY rats (1.85 +/- 0.10 versus 1.66 +/- 0.14 mg/dl; p = 0.28). In the control WKY rat strain, allopurinol therapy did not adversely affect weight gain or hematocrit and did not cause an increase in mortality. It resulted in a moderate decrement in kidney function (creatinine clearance: allopurinol-treated group 0.32 +/- 0.09 versus control group 0.46 +/- 0.04 ml/min/100 g body wt, in conjunction with mild-to-moderate tubulointerstitial inflammation (allopurinol-treated group 0.9 +/- 0.4 versus control group 0).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Feb
PMID:Nephrotoxicity of allopurinol is enhanced in experimental hypertension. 199 52

When Dahl salt-resistant (DR) rats are given mild post-deoxycorticosterone acetate (DOCA) hypertension, they will have, within 8 weeks, a 53% mortality on a high NaCl diet, without a rise of blood pressure. Forty-two DR rats were given DOCA in silicone (250 mg/kg) and 1% NaCl to drink. After 4 weeks, the DOCA and 1% saline were removed and replaced with a low NaCl diet and tap water. One week later, they were divided into two groups perfectly matched for blood pressure (154 mm Hg). One group had the aqueduct of Sylvius blocked with silicone and epoxy materials; the other group had a sham block. After 4 more recovery weeks on a low NaCl diet, blood pressure averaged 171 mm Hg in sham rats and 147 mm Hg in truly blocked rats (p less than 0.0001). Thus, the aqueduct block prevented most of the post-DOCA hypertension and permitted a strong post-DOCA recovery from the acute DOCA hypertension. The rats with the sham block had an actual rise in blood pressure during the post-DOCA recovery period. The vicious cycle leading to permanent post-DOCA NaCl hypertension was broken by the aqueduct block. Then both groups began an 8% high NaCl diet, and after 4 weeks, blood pressure averaged 184 mm Hg in sham and 155 mm Hg in truly blocked rats (p less than 0.0001). After 12 weeks on 8% NaCl, all sham rats had died (28 of 28), whereas only one of 14 truly blocked rats had died (93% reduction in mortality, p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jun
PMID:Aqueduct block markedly reduces mortality and hypertension in post-deoxycorticosterone acetate Dahl salt-resistant rats. 204 65


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