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

Arterial blood pressure and renal function of both clipped and non-clipped kidneys of benign two-kidney, one clip (2K1C) Goldblatt hypertension were evaluated in order to determine whether high-salt intake alters the course of the development and magnitude of hypertension or influences renal function. The administration of 0.9% sodium chloride as a drinking solution for 3 weeks suppressed plasma renin activity (PRA) and kidney renin content of the clipped kidney to normal values. Despite suppression of PRA and kidney renin content, the saline-drinking clipped rats still developed hypertension of the same magnitude as the water-drinking clipped rats. However, the onset of hypertension was delayed by 4 days. Urine flow, glomerular filtration rate (GFR) and sodium excretion rate from the clipped kidneys of the saline-drinking clipped rats were higher than the corresponding values in the water-drinking rats, and approached those observed in control animals. Thus, the high-salt intake which was associated with suppression of the activity of the renin-angiotensin system delayed the onset of, but not the final magnitude of, the hypertension. In addition, kidney function in the clipped kidneys of saline-drinking clipped rats was enhanced compared with that observed in the water-drinking clipped rats.
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PMID:Arterial pressure and renal function in two-kidney, one clip Goldblatt hypertensive rats maintained on a high-salt intake. 351 64

There is evidence that neither activation of the renin-angiotensin system nor changes in sodium balance can fully explain the maintenance of blood pressure in Goldblatt hypertension. Thus, in Goldblatt two-kidney, one clip hypertension in the rat sodium balance is negative and in hypertension of a few months' duration plasma renin initially elevated has returned to normal. When hypertension is reversed by removal of the constricting clip from the renal artery, blood pressure falls within a matter of hours even when hypertension has been present for many months, suggesting that the effect of structural changes in vascular resistance vessels has been overcome. In addition, blockade of the renin-angiotensin system during renal artery declipping does not influence the pattern of the blood pressure fall. We investigated the role of the renomedullary vasodepressor system by inducing medullary necrosis with 2-bromo-ethylamine hydrobromide. This causes a moderate blood pressure increase in normal rats, and partly inhibits the fall of blood pressure in Goldblatt two-kidney, one clip hypertension when the renal clip is removed. Chemical medullectomy is associated with a slightly negative sodium balance, plasma volume contraction, a reduction in plasma renin activity and urinary PGE2, and a minimal elevation in plasma vasopressin. Blood pressure elevation appears to be attributable to inhibition of a vasodepressor system based on the renal medulla. Chemical medullectomy offers a valuable tool for investigating the role of this medullary vasodepressor system.
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PMID:Vasodepressor mechanisms in experimental hypertension: studies using chemical medullectomy. 353 84

Increased glomerular capillary pressure (GCP) mediates glomerular damage in hypertension. The efficacy of captopril, an angiotensin converting enzyme (ACE) inhibitor, and captopril-hydrochlorothiazide (captopril-TZ) in lowering GCP and preventing glomerular damage was evaluated in rats with two-kidney, one clip (2K, 1C) Goldblatt hypertension and partial ablation of the unclipped kidney. Thirty days after surgery nine rats received captopril, 11 received captopril-TZ and eight served as untreated control rats. Sixty days later systemic hypertension was associated with increased GCP and severe structural damage in the unclipped kidney of C rats. Captopril lowered arterial pressure (AP), and prevented the rise in GCP and structural lesion. Captopril-TZ decreased AP and GCP to a greater extent, but did not reduce structural damage further. Captopril lowered GCP, preventing structural damage; greater reduction of GCP with captopril-TZ did not provide further protection.
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PMID:Effect of captopril and hydrochlorothiazide on glomerular haemodynamics and histological damage in Goldblatt hypertension with partial renal ablation. 355 76

The serum concentration of 7S collagen was measured radioimmunologically as a marker of basement membrane type IV collagen synthesis in diabetic and nondiabetic rats with Goldblatt hypertension. In non-diabetic rats the 7S collagen level was significantly raised after induction of hypertension (51%; p less than 0.001), and showed a positive correlation with relative heart weight as an integral parameter of hypertension (r = 0.63; p less than 0.01). In diabetic rats, which displayed a 7S collagen concentration roughly 2.5 times as high as the metabolically normal animals, the 7S collagen level was 27% higher in the hypertensive animals (p less than 0.01). There was no correlation with blood pressure or heart weight, but only a positive correlation with blood glucose (r = 0.51; p less than 0.05). The results indicate that haemodynamic alterations may alter basement membrane collagen metabolism. However, type IV collagen metabolism in diabetes is influenced to a greater extent by metabolic than by haemodynamic factors.
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PMID:Influence of hypertension on serum concentration of type IV collagen antigens in streptozotocin-diabetic and non-diabetic rats. 360 27

In two-kidney, one clip hypertensive rats renal cortical kallikrein was studied one and two weeks following induction of the hypertension in comparison with sham time controls. Cortical active kallikrein was lower in hypertensive rats only at week 2, although blood pressure was significantly higher one week after clipping. Total cortical kallikrein was however never different in sham control and in hypertensive rats. This results provide evidence for a change in the activation of prekallikrein during the onset of Goldblatt hypertension.
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PMID:Change in cortical active kallikrein during the onset of Goldblatt hypertension in the rat. 364 27

We investigated the ability of ouabain to produce lethal arrhythmias in rats with myocardial hypertrophy resulting from chronic renal hypertension. A gradual pressure overload was produced in female Wistar rats by left renal artery stenosis (two kidney, one clip, Goldblatt hypertension). Hypertension (systolic blood pressure greater than 150 mm Hg) developed within three weeks after clipping of the left renal artery and blood pressure continued to increase for the next five weeks. At ten weeks after the onset of hypertension animals were anesthetized with sodium pentobarbital (40 mg/kg) and artificially ventilated with room air while ECG was continually monitored and recorded. Continuous infusion of ouabain was maintained (0.7 mg/kg/min) through the inferior vena cava. Body weight and heart rate of control animals (C) was not significantly different from hypertensive (H) values, while systolic blood pressure in animals hypertensive for ten weeks was considerably greater (187 +/- 8.4 mm Hg) than their age-matched normotensive counterparts (123 +/- 6.0 mm Hg). Heart weight in hypertensive animals was elevated by 69% +/- 2.5 by time of study. Serological evaluation of both groups of animals revealed no significant differences in electrolytes and blood gases while significant differences were noted in glucose, BUN and creatinine. The average time to the first premature ventricular contraction was significantly shorter in H animals (3.5 +/- 0.2 min) when compared to C rats (6.0 +/- 0.2 min). The average time to ventricular tachycardia, ventricular fibrillation and death were also significantly shorter in H rats when compared to C animals (7.5 +/- 0.6 vs. 13.5 +/- 0.3; 13.5 +/- 0.5 vs. 21.0 +/- 0.5; 15.6 +/- 0.4 vs. 24.0 +/- 0.6 min). Thus, the hypertensive hypertrophied myocardium displays an increased propensity for lethal cardiac arrhythmias due to ouabain.
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PMID:Renal hypertensive hypertrophy in the rat: a substrate for arrhythmogenicity. 371 25

Neuropeptide Y content of the kidneys, heart, blood vessels, adrenals and brain stem was determined in both two-kidney, one-clip and one-kidney, one-clip Goldblatt hypertension in rats and compared with levels in age- and sex-matched controls. Renal neuropeptide Y content was significantly reduced in the clipped kidney of rats in both Goldblatt two-kidney, one-clip and Goldblatt one-kidney, one-clip models of hypertension. The content of neuropeptide Y was also reduced but to a lesser extent in the contralateral, non-ischaemic kidney in the two-kidney, one-clip model. In both models of hypertension, neuropeptide Y content in the heart was significantly reduced in the left ventricle and septum but unchanged in the atria and right ventricle wall. There was no significant change in the concentration of neuropeptide Y through the vasculature (major arteries and veins), including the renal artery distal to the clip, or in adrenals and brain stem.
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PMID:Neuropeptide Y in renovascular models of hypertension in the rat. 375

The innervation of basic renal structures (vascular glomerular pole with juxtaglomerular apparatus and renal tubules) was experimentally studied in rats at different stages of spontaneous and Goldblatt hypertension. Both fluorescent determination of adrenergic innervation and histochemical identification of cholinergic innervation have shown that they increased in spontaneous and remained unchanged in renal hypertension. The data obtained confirm an important role of intrarenal innervation in the development of kidney "resettings" in spontaneous hypertension.
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PMID:[Morphology of adrenergic and cholinergic innervation of the kidney as affected by spontaneous and ischemic renal hypertension in rats]. 377 95

The role of vasopressin (VP) in maintaining blood pressure in malignant two-kidney one-clip Goldblatt hypertension in chronically catheterized conscious rats was investigated by studying the effect of two structurally different VP pressor antagonists. Injections of either 20 micrograms/kg of dPTyr(Me)AVP or 10 micrograms/kg of d(CH2)5Tyr(Me)AVP failed to alter mean arterial pressure or heart rate, although both antagonists completely inhibited the pressor response elicited by exogenous VP. These results suggest, that VP is not involved as a pressor hormone in the maintenance of high blood pressure in this type of experimental hypertension.
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PMID:Effect of vasopressin blockade on blood pressure in conscious rats with malignant two-kidney Goldblatt hypertension. 384 65

Increased efferent renal sympathetic nerve activity could facilitate the development of hypertension by shifting the arterial pressure-renal sodium excretion curve to the right. Accordingly, interruption of the renal nerves should prevent the development of hypertension in animal models in which increased sympathetic nervous system activity has been implicated. Renal denervation delays the development of hypertension and results in greater sodium excretion in the Okamoto and New Zealand spontaneously hypertensive rat and in the deoxycorticosterone acetate-salt-treated rat, which suggests that these responses result from, at least in part, loss of efferent renal nerve activity. Similar sympathetically mediated renal vasoconstriction has been implicated in the pathogenesis of early essential hypertension in humans. The efferent renal sympathetic nerves play a diminishing role once hypertension is established in these models. Renal denervation in established one-kidney, one-clip and two-kidney, one-clip Goldblatt hypertension in the rat and chronic coarctation in the dog results in an attenuation of the hypertension. The depressor effect of renal denervation in these models is not caused by changes in renin activity or sodium excretion but is associated with decreased sympathoadrenal activity. These findings suggest that the afferent renal nerves contribute to the pathogenesis of renovascular hypertension by enhancing the activity of the sympathetic nervous system. Interruption of afferent renal fibers also appears to be the mechanism by which renal denervation prevents or reverses the normal increase in arterial pressure seen after aortic baroreceptor deafferentation in the rat.
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PMID:Renal nerves and hypertension: an update. 389 31


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