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

We attempted to produce two-kidney one-clip renovascular hypertension in SD rats, using hemoclips 0.2mm in diameter. After 12 weeks, 10 of the 16 rats were hypertensive. At this point, one-kidney, one-clip models were prepared by contralateral nephrectomy in five of the 10 hypertensive rats and in all six normotensive rats. Postoperatively, these 11 rats developed hypertension. Four to 6 weeks later, the clip was removed from the renal artery in five two-kidney and 11 one-kidney hypertensive rats. After unclipping, all the rats became normotensive although the extent of the fall in blood pressure in the one-kidney model was significantly greater than in the two-kidney model. The roles of the contralateral non-clipped kidney in the evolution of two-kidney, one-clip Goldblatt hypertension appear to be dual; sometimes depressing elevated blood pressure and sometimes maintaining it. Thus, it is postulated that in the six initially normotensive rats, its action was predominantly antihypertensive, while in the other 10 hypertensive rats, the presence of a contralateral non-clipped kidney served to develop and maintain hypertension even after unclipping.
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PMID:Study of renovascular hypertension in rats: I. The role of the contralateral, non-clipped kidney in two-kidney, one-clip hypertension in rats. 653 38

Changes in systolic blood pressure and urinary excretion of PGE2 and 6-keto PGF1 alpha 24 h after removing the renal artery clip were compared in one-kidney and two-kidney, one clip Goldblatt hypertension in the rat. Unclipping the one-kidney rat returned blood pressure to normotensive levels within 24 h and was associated with a substantial increase in urinary PGE2 and 6-keto PGF1 alpha. Although hypertension was also completely reversed in the two-kidney model there was no significant change in urinary prostaglandin excretion. Prior treatment with indomethacin (6.0 mg/kg) markedly reduced urinary prostaglandins after clip removal in both forms of hypertension but attenuated the fall in blood pressure in the one-kidney model only. There were no significant changes in urinary kallikrein activity following unclipping. It is suggested that in the one-kidney, one clip rat prostaglandins are released as the result of exposing the unclipped kidney to elevated arterial pressure and that these contribute to the subsequent fall in blood pressure.
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PMID:Release of prostaglandins during reversal of one-kidney, but not two-kidney, one clip hypertension in the rat. 657 Apr 85

Studies were performed on the cremaster skeletal muscle in rats to investigate the microvascular changes that are associated with established one-kidney, one clip (1K1C) and two-kidney, one clip (2K1C) Goldblatt hypertension and with deoxycorticosterone (DOC)-salt hypertension. Rats were anesthetized with urethane and chloralose; and cremaster muscles with intact circulation and innervation were suspended in a controlled Krebs bath. Microvascular pressures and vessel diameters were measured at three consecutive arteriolar (A) and venular (V) branch levels. Arteriolar diameters (means +/- SEM) in normotensive (NT) rats were 119 +/- 7, 86 +/- 5, and 31 +/- 3 micron respectively for 1A, 2A, and 3A arterioles; and venule diameters were 218 +/- 12, 141 +/- 15, and 53 +/- 7 micron respectively for 1V, 2V, and 3V venules. As compared to NT rats, there was a selective decrease in lumen size (percent reduction from control) for 1A and 2A (23% to 38%) in 1K1C and 2K1C rats and for 1A, 2A, and 3A (42% to 44%) in DOC rats. Venule diameters were not significantly different between normotensive and hypertensive animals at any branch level. Femoral artery pressures were significantly elevated (greater than or equal to 43%) in all three forms of hypertension; however, this increase in pressure was not proportionally transmitted throughout the microcirculation. This was evidenced by normal pressure in 3A arterioles and in all venules for 1K1C and 2K1C rats and by normal pressures in 3V and larger venules for DOC rats. Our findings indicate that elevated arterial pressure in chronic renal hypertension is not transmitted uniformly across all microvascular segments.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Distributions of microvascular pressure in skeletal muscle of one-kidney, one clip, two-kidney, one clip, and deoxycorticosterone-salt hypertensive rats. 669 46

Endothelial regeneration after a narrow, superficial aortic injury was studied in rats with chronic Goldblatt hypertension, genetic hypercholesterolemia, or a combination of hypertension and genetic hypercholesterolemia. In all groups, endothelial continuity was restored within 24 to 36 hours by a combination of endothelial migration and proliferation. A line of increased endothelial density covering the previous wound was seen through 16 weeks after injury. Intimal thickening after injury did not occur in any of the groups. These results indicate that hypertension and hypercholesterolemia neither delay endothelial regeneration nor cause intimal thickening after a small injury in the rat.
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PMID:Endothelial regeneration in hypertensive and genetically hypercholesterolemic rats. 684 20

Labetalol administered intra-gastrically in a dose of 30 mg/kg twice a day for 3 weeks significantly lowered systolic tail blood pressure (STBP) in chronic two-kidney Goldblatt hypertension in rats. Hypotensive response of labetalol in normotensive rats has also been demonstrated. Plasma renin activity (PRA) measured at the end of the treatment was similar in labetalol-treated and in dextrose-treated rats. The bradycardial response was evident in both hypertensive as well as in normotensive animals; however,, this change was statistically significant for the hypertensive rats only. Hypertension was associated with increase in the heart weight, which was not affected by labetalol treatment. Antihypertensive effect of labetalol is neither related to renin suppression nor to beta blockade.
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PMID:Effects of labetalol in chronic two-kidney Goldblatt hypertension (2-KGH) in rats. 699 Aug 87

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.
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PMID:Development of two-kidney Goldblatt hypertension in rats under dietary sodium restriction. 699 1

Attempted correction of two-kidney, one clip Goldblatt hypertension in the rat was carried out by three techniques; removal of the constricting clip, removal of the ischemic kidney, and converting enzyme blockade by oral captopril. Since duration of hypertension is said to be a critical factor, groups of rats were studied after short term (less than 6 weeks from clipping) and chronic (greater than 4 months) hypertension. Blood pressure, sodium balance, and plasma renin concentration (PRC) were followed before and after these correcting procedures. In a control group of animals, removal of a loose renal artery clip did not influence blood pressure and only caused trivial postoperative retention of sodium. Unclipping, however, normalized blood pressure in both short-term and chronic hypertension. After a major postoperative fall, blood pressure returned to somewhat elevated levels after nephrectomy in animals with chronic (but not short-term) hypertension. Sodium balance became markedly positive with the fall in blood pressure of operated hypertensive animals and was significantly correlated with the fall in blood pressure of operated hypertensive animals and was significantly correlated with the fall in blood pressure in these four groups at 7 days (r = 0.43). Captopril also produced a fall in blood pressure at 24 hours, with a positive sodium balance, although the relationship between blood pressure fall and sodium balance did not reach statistical significance (r = 0.30). The PRC was elevated in all hypertensive groups, although individual values overlapped with values from normal rats and nonhypertensive rats with a loose renal artery clip. The PRC fell to normal or subnormal values after either operative procedure and stabilized for at least 2 months independently of whether blood pressure fell or not. It is concluded that neither sodium retention nor renin hypersecretion maintains blood pressure in this model. Also, the rapidity of the blood pressure fall is not consistent with a role for vascular hypertrophy. The greater efficacy of unclipping suggests that the revascularized kidney after this procedure exerts a vasodepressor function independent of sodium excretion or the renin-angiotensin system.
Hypertension
PMID:Reversal of two-kidney one clip renovascular hypertension in the rat. 699 57

To determine the role of vasopressin in the maintenance of high blood pressure, the antihypertensive effect of the antagonists of the vasopressor effect of vasopressin, [1-deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin (dPVDAVP), and [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 4-valine, 8-D-arginine] vasopressin (cyclo dVDAVP), was studied in unanesthetized, nonsurgically stressed rats with adrenal regeneration hypertension, malignant DOCA-salt hypertension, and malignant two-kidney, one clip Goldblatt hypertension. The doses of vasopressin antagonist used blocked the blood pressure (BP) response to vasopressin almost completely, with no changes in the pressor response to norepinephrine and angiotensin II. Administration of the vasopressin antagonists did not induce significant changes in the mean BP in any of the three experimental groups studied. It is suggested that in unanesthetized, nonsurgically stressed rats with adrenal regeneration hypertension, malignant DOCA-salt hypertension, and malignant two-kidney, one clip Goldblatt hypertension, vasopressin does not have a role in the maintenance of high BP.
Hypertension
PMID:Evidence against a role of vasopressin in the maintenance of high blood pressure in mineralocorticoid and renovascular hypertension. 700 26

Several laboratories have reported evidence suggesting abnormalities in the activity of the sarcolemmal sodium pump in vascular smooth muscle in hypertension. The present experiments were designed to investigate the relationship of such changes to the status of the renin-angiotensin-aldosterone system and body fluid volumes. We assessed sodium pump activity in vitro in sodium-loaded tail artery and thoracic aorta freshly excised from rats with chronic one-kidney, one clip, and two-kidney, one clip hypertension, and from appropriate normotensive control rats. 86Rb uptake in the absence (total uptake) and presence of 1.0 mM ouabain (ouabain-insensitive uptake) was measured, and ouabain-sensitive uptake (nmole/mg dry weight/18 min) was calculated. There were increases in plasma renin activity in the two-kidney, one clip rats only. In the hypertensive rats there were significant increases (up to +60%) in the ouabain-sensitive and total 86Rb uptakes in both tail artery and aorta. The magnitude of increases in arterial tissue uptakes in the two forms of Goldblatt hypertension, and in one-kidney, one clip hypertensive rats given 0.9% saline to drink for 2 to 3 days before sacrifice, were similar. Further sodium loading of aortas from normotensive control rats did not increase their uptake. The results of this study provide no evidence for decreases in sodium pump activity, instead indicating that there are increases in the activity of the pump in the sarcolemma or arterial smooth muscle studied in vitro. These increases in pump activity do not appear to be related to altered activity of the renin-angiotensin-aldosterone system, to changes in body fluid volumes, or to increases in intracellular concentrations of sodium. Increases in numbers or concentration of sarcolemmal pump molecules or in their turnover rate may be involved. However, in vitro 86Rb uptake by tail artery and aorta may not reflect the status of sodium pump activity in resistance vessels in vivo.
Hypertension
PMID:Sodium pump activity in arteries of rats with Goldblatt hypertension. 703 34

Conscious rats with two-kidney one clip Goldblatt hypertension had the constricting clip removed during continuous infusion of either dextrose, saralasin, or captopril. Other dextrose-infused animals underwent removal of the ischemic kidney or a sham procedure. Direct arterial blood pressure (BP) was recorded throughout the 15-hour preoperative and subsequent 24-hour postoperative period. Rats were studied in the "early" phase (1-3 weeks duration) or "chronic" phase (greater than 4 months) of hypertension. Animals subjected to a sham procedure returned to preoperative BP values. The BP of animals unclipped or nephrectomized did not return to previous hypertensive levels. Instead, a biphasic response was seen where BP partially recovered from an operative fall and then slowly declined to normal at 24 hours; this effect occurred in both stages of hypertension. At 24 hours, removal of the ischemic kidney was as effective as removal of the constricting clip in the correction of both early and chronic phase hypertension. Rats infused with saralasin or captopril demonstrated an acute (within 2 hours) and sustained fall in BP, but not to normotensive levels. This fall was significant in all animals (p less than 0.01) apart from chronic phase rats infused with saralasin where no significant fall was seen. Although animals infused with saralasin or captopril commenced at a lower preoperative BP, the biphasic pattern of response to unclipping was identical to that of dextrose-infused unclipped rats. Thus, sustained inhibition of the renin-angiotensin system did not modify the correction of hypertension produced by removal of the constricting clip, and the response to surgical correction did not appear to be entirely mediated by changes in the activity of the renin-angiotensin system, particularly in the chronic stage. Equally, the rapidity of correction is not consistent with a role of vascular hypertrophy.
Hypertension
PMID:Surgical reversal of two-kidney one clip hypertension during inhibition of the renin-angiotensin system. 703 35


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