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

This study investigated the effects of treatment with desoxycorticosterone acetate and salt (DOCA/NaCl) on blood pressure, aortic vascular vasopressin receptors and in vitro vascular responsiveness in male rats. Four groups of animals were utilized in the study: a control group on normal tap water, a control group drinking a 1% NaCl solution; a DOCA/NaCl-treated group (1% NaCl in the drinking water); and a uninephrectomized (1K) DOCA/NaCl-treated group. DOCA/NaCl treatment for 4 weeks resulted in a significant elevation in blood pressure which was more pronounced in the uninephrectomized animal. The concentration of specific binding sites for vasopressin on the aorta were reduced in both the DOCA/NaCl-treated groups. However, the vascular responsiveness of the aorta to vasopressin was significantly reduced only in the hypertensive, uninephrectomized-DOCA/NaCl-(1K DOCA/NaCl) treated rat. Both the maximal contraction and the sensitivity was reduced in the 1K DOCA/NaCl group. The results of this study would suggest that the vascular alterations to vasopressin are probably post receptor mediated and result from the DOCA/NaCl-induced hypertension.
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PMID:Changes in vascular vasopressin receptors and responsiveness in DOCA/NaCl-treated rats. 296 70

Previous studies have shown that the spontaneously hypertensive rat (SHR) has a preference for 0.9% NaCl solution over water as a drinking fluid. This preference was decreased by chronic treatment of SHR with intracerebroventricular captopril (an angiotensin converting enzyme inhibitor). Although other strains of rats were compared to SHR, no studies, that we are aware of, have been reported in renal hypertensive rats. Wistar-Kyoto rats were sham operated or had a silver clip (i.d., 0.20 mm) placed on the left renal artery to produce renovascular hypertension. Three weeks later the rats were operated upon again to implant osmotic minipumps to deliver captopril or saline either into the right lateral brain ventricle (i.c.v.) or into the peritoneal cavity (i.p.). The rats had a choice of 0.9% NaCl or tap water during the study. Blood pressures were measured by a tail plysmographic method in the conscious rats. The rats that became hypertensive showed a marked preference for saline. Treatment with captopril i.p. (24 mumol/kg/day) stimulated preference for saline but i.c.v. treatment (24 mumol/kg/day) decreased the preference for saline despite reductions in blood pressure in both groups of renal hypertensive rats. These changes were not seen in renal hypertensive rats infused with saline. The results suggest that captopril's antihypertensive effect in this model of renal hypertension may be independent of the effects of the drug on preference to drink saline.
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PMID:Central angiotensin converting enzyme blockade and salt preference in renovascular hypertensive rats. 298 3

Angiotensin I converting enzyme inhibitors are typically classified as peripheral vasodilators. We studied the effect of captopril and a known vasodilator, hydralazine, on arterial pressure-urinary output relationships in adult spontaneously hypertensive rats to determine whether these drugs produced similar changes in this relationship. Tail-cuff pressure and 24-hour urine output and sodium excretion were measured under steady state conditions during ingestion of tap water or saline (1% NaCl) ad libitum. Sodium intake increased seven to nine times when rats drank saline, but in the absence of drug treatment, tail-cuff pressure was not altered significantly (water, 213 +/- 3 vs saline, 220 +/- 5 mm Hg). Daily administration of captopril (100 mg/kg p.o.) or hydralazine (15 mg/kg p.o.) for 2 weeks lowered tail-cuff pressure significantly (175 +/- 3 and 166 +/- 3 mm Hg, respectively; p less than 0.01) while rats drank tap water. Continued administration of hydralazine plus 2 weeks of drinking saline did not alter tail-cuff pressure (162 +/- 4 mm Hg), but with the addition of saline during captopril treatment, tail-cuff pressure was elevated significantly (210 +/- 5 mm Hg; p less than 0.01). Thus, hydralazine produced a parallel shift of the arterial pressure-urinary output relationship along the pressure axis. In contrast, captopril produced a marked change in the slope of this relationship, making arterial pressure extremely salt-sensitive. The results suggest that the two drugs have different effects on the mechanisms that contribute to the long-term control of arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Dec
PMID:Effect of captopril and hydralazine on arterial pressure-urinary output relationships in spontaneously hypertensive rats. 331 99

Pressor responses to arginine-vasopressin (AVP) and norepinephrine (NE) were studied in deoxycorticosterone (DOC)-salt hypertensive and prehypertensive rats. DOC-salt rats received weekly subcutaneous injection of DOC acetate (30 mg/kg) and given 1% saline for drinking. Salt and control rats received injections of sesame oil and given 1% saline or tap water, respectively. On the 5th day (prehypertensive stage) and at 6th week (hypertensive stage) after treatment had started, pressor responses were studied by measuring changes in mean arterial pressure recorded from the iliac artery in response to i.v. injections of AVP or NE under urethane anesthesia. Pressor response to AVP was enhanced both in DOC-salt hypertensive and prehypertensive rats compared with that in salt and control rats. Pressor response to NE tended to be enhanced in DOC-salt hypertensive rats, however, the enhancement was not observed in the rats in prehypertensive stage. Enhanced pressor response to AVP in DOC-salt prehypertensive rats was not due to the structural change of vascular beds, because peripheral resistance in isolated hindlimb preparations was similar in the three groups. Thus, pressor response to AVP was enhanced even in the prehypertensive stage in DOC-salt rats and the enhancement might be involved in the pathogenesis of hypertension in DOC-salt rats.
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PMID:Pressor response to vasopressin and norepinephrine in DOC-salt hypertensive and prehypertensive rats. 338 Dec 22

The effect of deoxycorticosterone (DOC)-induced hypertension on the calcium content within the aorta was studied before the increase in pressure (one week) and after the pressure had reached hypertensive levels (4 weeks). The volume density of free calcium detected ultrastructurally by pyroantimonate precipitation was quantitated by stereological techniques in aortic smooth muscle cells. An increase in the volume density of electron opaque precipitate was observed in the cytoplasm at one week of DOC treatment when neither the systolic blood pressure, the thickness of the media nor volume fraction of medial smooth muscle as compared to the extracellular space was increased significantly. The total aortic calcium as measured by atomic absorption spectroscopy was not increased at one week. By 4 weeks when the rats were hypertensive, the cytoplasmic free calcium in the smooth muscle cells and the number of peripherally-located cytoplasmic vesicles with precipitate was increased significantly. Total aortic calcium was also increased significantly in the DOC-saline group but not in the DOC group drinking tap water or in the saline drinking controls. An elevation of calcium within the cytoplasm of vascular smooth muscle cells may precede the development of hypertension and play a role in the pathogenesis of the increased blood pressure, increased medial thickness and hypertrophy of the vascular smooth muscle cells.
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PMID:Calcium distribution in aortic smooth muscle cells of deoxycorticosterone-hypertensive rats. A quantitative cytochemical study. 339 70

We have shown previously that the intracerebroventricular (icvt) infusion of 5 ng/h aldosterone (ALD) in the sensitized rat (one kidney removed, 1% NaCl plus 0.15% KCl solution to drink) produced hypertension similar in amplitude and time of onset to a 100-fold dose administered subcutaneously (s.c.), while a 5-ng/h subcutaneous infusion had no effect on blood pressure (BP). Dose-response studies on the icvt infusion of ALD were carried out in sensitized and non-sensitized (intact, with tap water to drink) male Sprague-Dawley rats (SDR). In both studies, a control group received the diluent, artificial cerebrospinal fluid (CSF), icvt. In sensitized rats, the pressures became significantly (P less than 0.05) elevated at day 7 in those receiving 15 ng/h icvt, day 11 in those receiving 5 ng/h icvt and 500 ng/h s.c. and day 18 in those receiving 1.5 ng/h icvt. The indirect systolic BPs at day 20 of infusion were 119 +/- 0.8 (s.e.) mmHg for controls, 182 +/- 5 for 15 ng/h icvt, 140 +/- 2 mmHg for 5 ng/h icvt, 131 +/- 1 mmHg for 1.5 ng/h icvt, 125 +/- 1 mmHg for 0.5 ng/h, and 159 +/- 5 mmHg for 500 ng/h s.c. Recovery (removal of pumps and return to water to drink) for 18 days resulted in the return of normal pressures in all groups except the 15 ng/h, icvt group in which pressures remained slightly, but significantly elevated at 127 +/- 3 mmHg. In non-sensitized rats, the pressures became significantly elevated in animals receiving 45 ng/h icvt and 1 microgram/h s.c. by day 14.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dose-response studies of intracerebroventricular infusion of aldosterone in sensitized and non-sensitized rats. 341 Nov 22

The effect of adrenalectomy on renin secretion was investigated in conscious rats with glucocorticoid-induced hypertension. Adrenalectomized and sham-operated rats were made hypertensive with methylprednisolone acetate (20 mg/kg s.c. once/week X 2 weeks) supplemented with deoxycorticosterone pivalate (10 mg/kg s.c. once/week X 2 weeks). During the 2 week developmental phase of hypertension, tap water or isotonic saline was given as drinking fluid to respectively 10 and 13 adrenalectomized rats and 10 and 11 sham-operated rats. On the day of the acute administration of captopril or vehicle there was no significant difference in body weight, mean blood pressure, heart rate, serum electrolytes and plasma norepinephrine levels between the 4 groups of rats. Circulating epinephrine could not be detected in adrenalectomized rats. Plasma renin activity was markedly higher in adrenalectomized rats than in the sham-operated rats even after sodium supplementation. Captopril (10 mg/kg i.v.) produced no significant blood pressure lowering effect in rats given tap water to drink, either adrenalectomized (n = 11) or sham-operated (n = 10). These findings indicate that the activation of the renin-angiotensin system in adrenalectomized rats with glucocorticoid-induced hypertension is not directly mediated by the development of adrenal failure. They also show that the maintenance of high blood pressure in this form of experimental hypertension is not significantly enhanced when renin secretion is stimulated by adrenalectomy.
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PMID:Regulation of renin secretion in conscious adrenalectomized rats with glucocorticoid-induced hypertension. 352 16

This study investigated vascular responsiveness in stroke-prone spontaneously hypertensive rats (SHRSP) and the effect of antihypertensive treatment on this responsiveness. Weanling (4-week-old) male and female SHRSP and Wistar-Kyoto rats (WKY) received either the antihypertensive combination treatment of hydralazine plus hydrochlorothiazide in drinking water or tap water alone (controls) for 15 weeks. Whereas the antihypertensive combination prevented the development of hypertension in treated SHRSP (SHRSP-T), blood pressure remained unchanged in treated WKY (WKY-T). Femoral arterial smooth muscle responsiveness to KCl, norepinephrine, and calcium (in the presence of either 40 mM KCl or 1 microM norepinephrine) was not altered in SHRSP when compared with WKY. A significant increase in the sensitivity of femoral arteries to KCl and calcium (in the presence of 40 mM KCl) was seen, however, in SHRSP-T and WKY-T. An increased sensitivity to norepinephrine and calcium (in the presence of 1 microM norepinephrine) was seen only in SHRSP-T. Isoproterenol-induced relaxation was significantly attenuated in both SHRSP and SHRSP-T. Relaxation induced by sodium nitroprusside and calcium (membrane stabilization) was not different between the four groups. These results show that femoral arterial smooth muscle responsiveness to vasoconstrictor stimuli is not altered in SHRSP but that beta-adrenergic-mediated relaxation is attenuated. Antihypertensive treatment resulted in an enhanced responsiveness to these vasoconstrictor stimuli but had no effect on the relaxation properties of femoral arterial smooth muscle.
Hypertension 1987 May
PMID:Vascular reactivity in the spontaneously hypertensive stroke-prone rat. Effect of antihypertensive treatment. 357 Apr 24

Uninephrectomized male Munich-Wistar rats received either weekly subcutaneous injections of vehicle and water for drinking; injections of desoxycorticosterone (DOC) and 1% saline (SALT) for drinking; or DOC and SALT with hydrochlorthiazide, hydralazine, reserpine and KCl added. All studies were performed six weeks after UNX. At that time, rats receiving DOC and SALT alone were hypertensive and had significantly more proteinuria and morphologic evidence of glomerular injury than rats given vehicle and tap water which were normotensive. Antihypertensive therapy normalized mean arterial pressure in DOC-SALT rats, but failed to prevent proteinuria, mesangial expansion or focal segmental glomerular lesions. Micropuncture studies revealed that glomerular capillary pressure was elevated in both untreated and treated DOC-SALT animals. We conclude that drugs which successfully reduce systemic blood pressure may fail to correct glomerular capillary hypertension in DOC-SALT rats. As persistence of intrarenal hypertension is associated with significant glomerular injury, normalization of glomerular capillary pressure rather than systemic arterial pressure is crucial to the prevention of glomerular injury in this model.
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PMID:Glomerular hypertension and injury in desoxycorticosterone-salt rats on antihypertensive therapy. 357 36

Chronic and recurrent choroidal (ciliochoroidal) detachments developed following glaucoma filtration surgery in 14 eyes of 13 patients during a 9-year period. Three specific subgroups were identified: recurrent, inflammatory, and chronic (present for more than 6 months). The factors that may be related to the development of chronic and recurrent choroidal detachments included patient age (mean, 68.8 years), systemic hypertension or atherosclerotic heart disease, hyperopia, aqueous suppressant therapy, ocular inflammation, and full-thickness filtration surgery. A total of 46 choroidal detachments in 14 eyes were recorded and required drainage of suprachoroidal fluid on 34 occasions. All eyes developed visually significant cataracts, and complete resolution of the recurrent or chronic choroidal detachment occurred following cataract extraction in six eyes. Treatment of chronic and recurrent choroidal detachments should include intense therapy of ocular inflammation, discontinuation of medications that can incite ocular inflammation, discontinuation of topical and systemic aqueous suppressant therapy, and when a visually significant cataract is present, cataract extraction combined with a choroidal tap should be performed.
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PMID:Chronic and recurrent choroidal detachment after glaucoma filtering surgery. 357 81


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