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

The increase in plasma renin activity induced by captopril is used in the clinical evaluation of renovascular hypertensive patients. This increase in plasma renin activity could result from either the concomitant fall in systemic pressure or other effects of captopril, such as the removal of an angiotensin II inhibitory effect on renin release, the increased production of bradykinin or prostaglandins, etc. To examine the effect captopril has on plasma renin activity, independent of changes in systemic pressure, captopril (5, 10 and 50 micrograms/kg iv) was administered to conscious dogs before and following the development of 1 clip-2 kidney Goldblatt hypertension. Plasma renin activity, under normal conditions remained unchanged, while during hypertension it increased 2.0, 2.8 and 3.5 fold respectively in response to the three doses of captopril. These results suggest that the development of renovascular hypertension sensitized the kidney to release renin when challenged by captopril and that the effect is independent of changes in systemic pressure.
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PMID:Stimulation of plasma renin activity by captopril in renovascular hypertensive conscious dogs. 265 Sep 28

Evidence from animal studies demonstrates that the renin-angiotensin (ANG II) system and sodium retention play major roles in experimental renovascular hypertension (RVH). Two basic models have been described. In the first, one-clip two-kidney Goldblatt hypertension, the ischemic kidney secretes renin, which leads to increased ANG II formation and hence elevation of blood pressure (BP). As BP rises, sodium excretion by the intact contralateral kidney increases (pressure natriuresis); therefore, there is no sodium retention. In the second, one-clip one-kidney Goldblatt hypertension, the contralateral kidney is removed. In this case the pressure natriuresis can no longer occur, and sodium retention occurs. The ensuing expansion of plasma volume inhibits renin secretion, so that in this model the renin level is normal or low. Following the clipping of the renal artery, renal blood flow and pressure are maintained distal to the stenosis by an ANG II-mediated vasoconstriction. This acts preferentially on the efferent glomerular arterioles, so that the ratio of preglomerular to postglomerular resistance is reduced, which helps to maintain glomerular filtration despite the reduced renal perfusion pressure. In the contralateral kidney the afferent arteriolar resistance is increased, probably as a direct result of exposure to the higher intrarenal arterial pressure. ANG II constricts the efferent arterioles in the same way as in the ischemic kidney, so that the ratio of preglomerular to postglomerular resistance is unchanged. When an angiotensin converting enzyme (ACE) inhibitor is given, the efferent arterioles vasodilate. In the ischemic kidney this may produce a reduction of glomerular filtration rate (GFR), which is not seen in the contralateral kidney. Unilateral RVH in humans corresponds closely to the animal model of one-clip two-kidney hypertension. Plasma renin activity is usually high, and converting enzyme inhibitors lower BP effectively. The increased renin is due exclusively to increased secretion of renin by the ischemic kidney, and is completely suppressed in the contralateral kidney. It is not clear whether bilateral RVH corresponds to the one-clip one-kidney model, but there is circumstantial evidence to suggest that both renin and volume factors may be involved. The majority of cases of human RVH are caused by atheroma, which is commonly bilateral, or by fibromuscular dysplasia. The former tends to be associated with atheroma elsewhere in the arterial tree, and often progresses to complete occlusion and renal failure. The latter occurs in younger patients, and almost never progresses to complete occlusion.
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PMID:Renovascular hypertension: etiology and pathophysiology. 265 13

These studies were aimed at investigating whether chronic hypertension in pregnancy causes changes both in salt excretion (NaE) and in glomerular hemodynamics. Metabolic and renal micropuncture studies were performed in pregnant (P) and Virgin (V) Munich-Wistar rats with normal blood pressure (N) and two-kidney Goldblatt hypertension (H). Mean NaE was higher in PN than VN (2.7 vs. 1.7 meq/day, P less than 0.01). Hypertension raised NaE both in P and V rats: in P and V rats with "benign" hypertension (blood pressure less than 180 mmHg) NaE averaged 3.2 and 2.6 meq/day, respectively (P less than 0.05); mean NaE was 5.9 and 3.8 meq/day, respectively (P less than 0.01), in P and V rats with "malignant" hypertension (blood pressure greater than or equal to 180 mmHg). Afferent arteriole resistance (Ra) averaged 1.73 and 3.50 10 dyn.s-1.cm5 in PN and VN, respectively (P less than 0.01). Hypertension raised Ra in V, but not in P rats (4.47 vs. 2.14 10 dyn.s-1.cm5, P less than 0.01). Thus glomerular plasma flow, glomerular capillary hydrostatic pressure, and single-nephron glomerular filtration rate were markedly higher in PH than VH rats: in PH rats single-nephron filtration fraction was significantly lower than in VH. These results show that in PH rats a marked rise in NaE is associated with glomerular vasodilation.
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PMID:Glomerular dynamics and salt balance in pregnant rats with renal hypertension. 270 42

The effects of one-kidney, one clip Goldblatt hypertension on aortic atherosclerosis have been studied in the Watanabe heritable hyperlipidemic (WHHL) rabbit. Renovascular surgery was performed on WHHL rabbits at 3 months of age, and the rabbits were followed for periods of 3-6 months. Aortic atherosclerosis was assessed by measurement of intimal surface involvement with atherosclerotic lesions, determination of aortic free and ester cholesterol content, and microscopic examination. Systolic blood pressure increased by approximately 40-60 mm Hg in the renovascular surgical group as compared with the sham-operated group, but body weight, heart rate, serum cholesterol, and serum triglyceride were unaffected. Aortic atherosclerosis was increased in the hypertensive rabbits, even after 2-3 months of hypertension. At 3 months after renovascular surgery, the aortic surface area covered by atherosclerotic disease averaged 77 +/- 4.4% in hypertensive as compared with 16 +/- 3.3 in control rabbits. At 6 months after surgery, the values were 62 +/- 8.2% and 30 +/- 5.3% in the hypertensive and control rabbits, respectively. The differences in surface involvement and cholesterol content as a result of hypertension were particularly prominent in the descending thoracic aorta. Atherosclerotic lesions in the descending thoracic and abdominal aortic regions of normotensive WHHL rabbits were localized primarily to the ostia of branch vessels, but in the hypertensive rabbits, the involvement was typically very diffuse. No major differences in the nature of atherosclerotic lesions of comparable size were apparent by light microscopy. The results indicate that hypertension accelerates atherogenesis in the WHHL rabbit and suggest that this model may be valuable for studying the mechanisms by which such acceleration is induced.
Hypertension 1989 Aug
PMID:Influence of hypertension on aortic atherosclerosis in the Watanabe rabbit. 275 79

Vascular reactivity of the contralateral kidney of conscious Goldblatt hypertensive dogs was studied by eliciting renal blood flow (RBF) responses to intra-arterial infusions of vasoconstrictor and vasodilator agonists in control sessions and at weekly intervals postclipping. Systemic arterial blood pressure (BP) and RBF were monitored during each recording session via an implanted catheter and electromagnetic blood flow probe, respectively. BP was maximally increased within 1 wk and remained elevated for the duration of the study. The relationship between the negative percent change in RBF (-% delta RBF) and the renal arterial plasma concentration of adrenergic agonists, angiotensin II and thromboxane mimetic (U 46619), infused intra-arterially was subjected to regression analysis, and 25 and 50% effective doses (ED25 and ED50, respectively) were calculated. Vascular sensitivity to phenylephrine and norepinephrine increased within a month or more of hypertension. Vascular reactivity to angiotensin II was unchanged. In contrast to the delayed increase in renal vascular reactivity to adrenergic agonists, enhancement of the RBF responses to U 46619 was seen within 1-2 wk. In addition, beta-adrenoceptor-mediated vasodilation appeared suppressed during hypertension. Alteration in the response of the contralateral kidney to both vasoconstrictor and beta-adrenoceptor-mediated vasodilator stimuli may contribute to renal hemodynamic changes in Goldblatt hypertension.
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PMID:Renal vascular reactivity to U 46619 and adrenergic agonists in Goldblatt hypertension. 289 20

It has been much discussed whether left ventricular hypertrophy (LVH) in hypertension implies improved or impaired cardiac performance, mainly because experiments in various hypertensive models have given controversial results. It has, for example, been suggested that increased collagen content may depress LV function both in renal and spontaneous hypertension (SHR) in rats. For such reasons cardiac performance was studied both in SHR and in normotensive control rats (NCR) before and during superimposed two-kidney, one clip Goldblatt hypertension, and also 1 week after reversal of hypertension by unclipping. The LV function of the isolated hearts was determined in an antegrade working heart perfusion system. Further, myocardial morphology, with regard to fibrous tissue infiltration and energy metabolic status, were evaluated in the renal hypertensive rats before and after unclipping. Compared with NCR, maximal cardiac performance was elevated in the hypertrophied SHR hearts, but depressed when renal hypertension was superimposed, even though this led to further LVH. However, one week after reversal of renal hypertension, when LVH was still considerable, cardiac function was increased well above the control level, even though the stores of high energy compounds and the content of myocardial fibrous tissue was almost the same as during renal hypertension. It is concluded that LVH generally enhances cardiac performance, but that concomitant renal hypertension exerts a cardio-depressive influence which can neither be ascribed to an increased fibrous tissue content nor to a reduced energy charge potential. It is therefore suggested that some negative inotropic agent of renal or extrarenal origin is released during two-kidney, one clip renal hypertension, which offsets the enhanced performance induced by the left ventricular hypertrophy.
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PMID:Functional, morphological and metabolic characteristics of isolated hearts from normotensive and spontaneously hypertensive rats before, during and after renal hypertension. 293 89

Renal damage is systemic hypertension has traditionally been related to an ischemic glomerular injury secondary to arteriosclerosis and arteriolosclerosis of preglomerular vessels. The use of micropuncture techniques with histopathologic studies have suggested non ischemic mechanisms of renal damage in systemic hypertension. Indeed in experimental models of hypertension which include DOCA-Salt, Goldblatt hypertension or genetic hypertension, the development of glomerular damage is associated with hyperfiltration secondary to increases in flow and pressure to the glomerular capillary. Hyperfiltration as a mechanism of renal damage in human systemic hypertension has not been established. Recent studies from our group have demonstrated lack of renal functional reserve in patients with systemic hypertension, reserve which is reestablished after 3 days of antihypertensive treatment. These data suggest therefore the presence of hyperfiltration as a possible mechanism of renal damage in patients with essential hypertension.
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PMID:[Is the kidney lesion caused by hypertension really ischemic?]. 294 50

Since various studies suggest that chronic physical conditioning promotes myocardial vascularity, we investigated whether it could prevent the coronary reserve abnormalities of hypertensive cardiac hypertrophy. One week after operation, female Sprague-Dawley rats with two-kidney, one clip Goldblatt hypertension were either subjected to a moderate exercise program by swimming (n = 21) or kept sedentary (n = 16) for 9 weeks. Sedentary (n = 16) and exercised (n = 15) sham-operated rats served as controls. Maximal coronary blood flow and minimal coronary resistance, either per unit mass or for the entire left ventricle, an index of the functional cross-sectional area of the coronary resistance vessels, were determined in conscious, unrestrained rats by left atrial microsphere injection following maximal vasodilation with carbochrome (12 mg/kg). Following exercise, left ventricular mass was moderately (+5-10%) but significantly increased in normotensive rats, whereas left ventricular hypertrophy was significantly accentuated in the hypertensive rats. Minimal coronary resistance for the entire left ventricle was significantly decreased (-24%) in normotensive rats but did not change significantly in hypertensive rats. Minimal coronary resistance per unit mass (the coronary vasodilator reserve) tended to decrease in normotensive rats (-17%), whereas it tended to be further augmented in hypertensive rats (+13%). However, these differences were marginally significant and were not associated with any changes in maximal coronary blood flow per unit mass (the coronary flow reserve). Thus, in normal rats, exercise promoted myocardial arterial vascularity in parallel with the development of cardiac hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Jul
PMID:Effects of chronic exercise on the coronary circulation in conscious rats with renovascular hypertension. 295 5

The influence of isoenzyme pattern of myosin on cardiac energetics was investigated in a modified in situ heart-lung preparation in the rat. Chronic pressure load (spontaneous hypertension, aortic stenosis, Goldblatt hypertension), intermittent feeding, and swim-training elicited redistribution in the concentration of alpha chains of myosin ranging from 18 to 94%. The influence of isoenzyme pattern of myosin on cardiac energetics could be quantitatively assessed by extrapolation of the regression line of oxygen and substrate consumption related to tension time index. Fast myocardium with 100% alpha chains had an ATP and oxygen consumption which exceeded that of slow myocardium with 0% alpha chains by about 60%. This corresponds well to the state of activity of myofibrillar ATPase of fast myocardium which also exceeds that of slow myocardium by about 50%. Furthermore it could be shown that acute increase in the ATPase activity depends on the isoenzyme pattern of myosin. Under the influence of catecholamines the oxygen consumption related to tension time index increased by 30-40% in fast myocardium, whereby in a myocardium with 40% alpha chains no increase in oxygen consumption per unit tension time index was observed, when catecholamines were applied.
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PMID:Implications of myocardial transformation for cardiac energetics. 295 58

In a previous study we demonstrated ventricular hypertrophy in male but not in female sinoaortic denervated rats. To evaluate a possible sexual influence on ventricular hypertrophy of other models for experimental hypertension, we studied two-kidney one clip and one-kidney one clip Goldblatt hypertension. The results showed left ventricular hypertrophy in male but not in female two-kidney one clip groups, despite the same arterial hypertension level in both groups. In the one-kidney one clip groups, left ventricular hypertrophy was greater in male than in female rats. The results indicate a sexual influence in ventricular hypertrophy when the arterial renovascular hypertension level is moderate.
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PMID:Left ventricular hypertrophy differences between male and female renovascular hypertensive rats. 297 86


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