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

Renin-like activity can be demonstrated in arterial extracts from normal rats and from rats with Goldblatt hypertension. We have found no evidence, however, for elevated arterial renin levels in relation to plasma renin activity. Studies of the reversal of renovascular hypertension indicate that the fall in blood pressure produced by renal artery deconstriction is not renin-dependent. However, molecular biological techniques indicate that extrarenal renin gene expression is altered in some tissues, such as the adrenal gland in Goldblatt hypertension, and it is possible therefore that extrarenal renin synthesis is important in blood pressure control. This has to be distinguished from renin derived from plasma uptake.
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PMID:The role of extrarenal renin in Goldblatt hypertension. 174 94

Renal functional reserve (renal response to protein loading, RFR) has been suggested as a method to verify the presence of hyperfiltration. This study was designed to evaluate the role of RFR as an indicator of increased glomerular capillary hydrostatic pressure in short-term treated and untreated rats with two-kidney, one-clip Goldblatt hypertension. One month after placing a silver clip, micropuncture studies were performed on the unclipped kidney. Normal rats and three groups of clipped rats [untreated group (HYP), a group treated with captopril (CEI) and a group treated with verapamil (VER) 5 days before the micropuncture studies] were studied. Glomerular hemodynamics and proximal tubular reabsorption were measured in control period and during intravenous administration of glycine (G). In normal rats, G produced afferent and efferent dilation, increases in single nephron plasma flow (SNPF) and single nephron glomerular filtration rate (SNGFR) of 24%. Systemic hypertension in HYP rats was associated with increases in transcapillary pressure gradient (delta P) and SNGFR. In this hyperfiltration state, infusion of G did not modify SNGFR of SNPF defining loss of RFR. The antihypertensive treatment was equally effective in normalizing MAP and delta P in CEI and VER, but only CEI rats responded to G with a 20% increase in SNGFR due to an increase in delta P. The most striking findings were that loss of RFR in both HYP and VER rats was associated with a significant decrease in absolute and proximal fractional reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal functional reserve in treated and untreated hypertensive rats. 178 41

Vascular pressures were measured in the principal (A1) arteriole and in upstream small arteries of the rat cremaster muscle to investigate vascular resistance changes associated with one-kidney, one clip Goldblatt hypertension. Pressure measurements were made at a proximal and distal site of each vessel using a servonull micropipette system. Vessel diameters were measured using video microscopy. A1 arteriole and external spermatic artery diameters were both decreased after 2 and 4 weeks of hypertension. Mean arterial pressure was elevated after 2 weeks of hypertension (106 +/- 4 mm Hg versus 140 +/- 5 mm Hg). Likewise, vascular pressures were elevated at every site: pudicepigastric artery (36%), external spermatic artery (47%), and A1 arteriole (38%). The pressure drop along the external spermatic artery was increased (87%) after 2 weeks of hypertension. Mean arterial pressure was further elevated from 2-4 weeks of hypertension (105 +/- 4 mm Hg versus 162 +/- 7 mm Hg) but only the proximal pudic-epigastric artery pressure was further elevated during this time from 2 to 4 weeks (131 +/- 5 mm Hg versus 147 +/- 7 mm Hg) of hypertension development. This was associated with an increased pressure drop (87%) along the artery compared with the situation at 2 weeks. These data indicate that small arteries upstream from the microcirculation contribute significantly to the increase in vascular resistance during hypertension. In addition, these data indicate that the increases in small artery resistance do not develop uniformly throughout all vessel branches.
Hypertension 1991 Mar
PMID:Small artery resistance increases during the development of renal hypertension. 199 62

Effects of a high-salt diet on blood pressure, extracellular fluid volume, and the renin-angiotensin system in rats with the two types of Goldblatt hypertension were examined. Both in one-kidney, one clip (1K1C) rats and in one-kidney, sham-clipped (1K) rats, systolic blood pressures of rats which received a high-salt diet for 4 weeks were higher than those of rats of respective groups on a normal-salt diet, suggesting an increased sensitivity of blood pressure to changes in salt intake. Whereas sodium space was increased in 1K rats on the high-salt 1K1C rats receiving the high-salt did not have significantly increased sodium space. These results suggest that acceleration of 1K1C hypertension with salt load could not be explained only by changes in extracellular fluid volume. In contrast, both in two-kidney, one clip (2K1C) rats and in two-kidney, sham-clipped (2K) rats, the high-salt diet produced no change in blood pressure despite the increase in sodium space, suggesting a decreased salt sensitivity. Although on the normal-salt diet the blood pressure of 2K1C rats tended to correlate with plasma renin activity, on the high-salt diet plasma renin activity was markedly decreased, and then blood pressure highly correlated with sodium space. Accordingly, the lesser salt sensitivity in 2K1C rats is probably attributable to the counterbalance of the suppressed renin-angiotensin system against volume expansion. Evidence presented suggests, therefore, that 1K1C rats have greater salt sensitivity of blood pressure than 2K1C rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Salt sensitivity in Goldblatt hypertensive rats--role of extracellular fluid volume and renin-angiotensin system. 202 87

Renovascular hypertension has its experimental counterpart in the two-kidney, one clip model (Goldblatt hypertension). From the study of this model, a general pathophysiological scheme has evolved suggesting that temporal stages in the development and maintenance of hypertension are regulated by complicated hormonal and neural interrelations. The central roles played by the renin-angiotensin system and the renal nerves is discussed as they relate to other hormones. In addition, the possible contribution of converting enzyme inhibitors to understanding the pathophysiology of this condition is discussed.
Hypertension 1991 May
PMID:Pathophysiology of renovascular hypertension. 202 13

In order to investigate the consequences of different types of cardiac hypertrophy on myocardial capillary and fibrosis density in rats we describe here, in the same hearts, the pattern of capillary bed density visualized by fluorescein isothiocyanate dextran (FITC-dextran) and the pattern of fibrosis density as determined by automated image analysis. Pressure overload was induced by clipping one renal artery in rats (one-clip, two-kidney Goldblatt hypertension, RHV). Volume overload was induced by creation of an arteriovenous shunt between the abdominal aorta and the vena cava (aorto-caval fistula model ACF). Animals were sacrified at 1, 3 and 6 months following surgical procedure. Immediately prior to sacrifice, FITC-dextran (MW 150,000) was injected with the animal under ether anesthesia. Five minutes later, cardiac diastolic arrest was induced by the i.v. injection of potassium chloride. The heart was rapidly excised and placed in a formaldehyde solution. The degree of cardiac hypertrophy was calculated after measurement of cardiac weight. Left ventricular wall thickness and cavity area were measured by microscopic methods. Capillary density and geometry were determined by morphometric methods, under ultraviolet light microscopy, using a graphic tablet connected to a microcomputer. The degree of myocardial fibrosis, visualized with Sirius Red, was estimated by the use of automated image analysis using light microscopy. In renovascular hypertension, cardiac hypertrophy was maximum at one month (36%) and persisted through the six months of the study. This increase in cardiac mass was concentric, due to a significant increase in ventricular wall thickness and was associated with a marked increase in fibrosis and a significant decrease in subendocardial capillary density. These effects existed already one month and did not change with time. In the aorto-caval fistula model, cardiac hypertrophy was also maximum at one month (+56%), but this eccentric increase in cardiac mass was associated with no significant change in left ventricular wall thickness, but rather with a significant increase in the surface area of the left ventricular cavity. This volume overload hypertrophy was associated with a decrease in subendocardial capillary density which was negatively correlated with time. In contrast to concentric hypertrophy there was no increase in the fibrosis density compared to the sham-operated groups. Despite the identical degrees of hypertrophy, pressure and volume cardiac overload differed in a significant manner in both left ventricular wall thickness and cavity surface area.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Morphometric analysis of collagen network and plasma perfused capillary bed in the myocardium of rats during evolution of cardiac hypertrophy. 242 67

This study examined the role of the lipoxygenase (LO) pathway in the maintenance of hypertension in rats with two-kidney, one clip (2K,1C) Goldblatt hypertension. A single dose of the lipoxygenase blocker phenidone was injected intraperitoneally to 2K,1C rats during the early phase (14 days) of the development of hypertension (mean intraarterial blood pressure 137 +/- 3.9 mm Hg). Phenidone (60 mg/kg) markedly decreased arterial pressure to nadir levels of 58.9% of resting blood pressure. The maximal changes were observed 15 min after injection and the hypotensive response was sustained for at least 2 h. Plasma renin concentration (PRC) increased from 74.3 +/- 18.9 to 281.0 +/- 6.5 ng/mL/h after injection (P less than .05). Thus, the hypotensive effect of phenidone was not due to suppression of renin secretion but presumably due to inhibition of its effects. It is suggested that arachidonate metabolites of the LO pathway at the vascular bed may be involved in maintenance of high arterial pressure in 2K,1C renovascular hypertension in rat.
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PMID:Hypotensive effects of the lipoxygenase inhibitor phenidone in two-kidney, one clip Goldblatt hypertension. 251

To investigate the response of cardiac collagen to arterial hypertension and its reversal, we measured the hydroxyproline concentration in all parts of the rabbit heart in three groups: a chronic hypertension group (n = 11), a reversal group (n = 9) and an age-matched control group (n = 10). Left ventricular overload was produced by one-kidney, one-clip Goldblatt hypertension and its reversal was produced by clip release. The wet weight of every part of the left side of the heart was increased by hypertension and all parts except for the papillary muscles showed regression with reversal. However, the response of collagen was quite different among the various parts of the heart. The wet weights of the left atrium, left ventricular free wall, interventricular septum, and anterior and posterior papillary muscle in the hypertension group were 144 (P less than 0.01), 140 (P less than 0.01), 134 (P less than 0.01), 144 (P less than 0.01) and 129% (P less than 0.01), respectively, and those in the reversal group were 92, 113 (P less than 0.05), 107 (P less than 0.05), 142 (P less than 0.05) and 126% (P less than 0.05) of those in the control group, respectively. Hydroxyproline concentrations in the respective parts in the hypertension group were 79 (P less than 0.05), 91, 98, 121 (P less than 0.05) and 120% (P less than 0.05) and those in the reversal group were 86, 93, 94, 107 and 110% of those in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hydroxyproline in all parts of the rabbit heart in hypertension and in its reversal. 253 38

alpha-Adrenergic receptor subtypes were investigated using [3H]prazosin, an alpha 1 selective antagonist, and the alpha 2 selective antagonist [3H]rauwolscine in a smooth muscle plasma membrane enriched microsomal fraction prepared from rabbit intrarenal arterial vasculature. Both radioligands displayed single components on Scatchard analysis. The specific binding of [3H]prazosin was of high affinity (0.54 +/- 0.04 nM) with a maximum binding capacity (Bmax) of 212 +/- 15 fmol/mg protein. The maximum number of [3H]rauwolscine binding sites was 64 +/- 4 fmol/mg of protein with a dissociation constant (Kd) of 5.60 +2- 0.27 nM. Binding of both radioligands was rapid, saturable, and specific. alpha 1- and alpha 2-adrenergic receptors in the intrarenal arterial membrane preparation were also characterized at 2-, 4-6-, and 10-12-week intervals during the course of development and maintenance of chronic two-kidney, one clip (2K1C) Goldblatt hypertension and in age-matched sham-operated normotensive control rabbits. The alpha 1-adrenergic receptor affinity for [3H]prazosin binding in hypertensive rabbits was significantly increased in the stenotic, but not contralateral, kidney at 2 weeks; however, at 6 weeks the receptor affinity of both kidneys was significantly increased compared with those of the normotensive control group. No difference in alpha 1-adrenergic receptor affinity was seen at 12 weeks, and there were no changes in Bmax at any of the weekly intervals. Neither the Kd, nor Bmax, for [3H]rauwolscine in either kidney showed a significant difference between hypertensive rabbits and normotensive control rabbits. These studies demonstrate the existence in the rabbit intrarenal arterial vasculature of binding sites with alpha 1- and alpha 2-adrenergic receptor specificity.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Jun
PMID:Characterization of intrarenal arterial adrenergic receptors in renovascular hypertension. 254 25

The effect of clipping the left renal artery on left and right kidney renin mRNA levels during the early and chronic phases of two-kidney, one clip Goldblatt hypertension in the rat was studied. Renin mRNA levels were determined using northern and dot blotting. Four weeks after clipping, renin mRNA levels were sixfold higher in the left kidney and eightfold lower in the right kidney of the Goldblatt rats compared with the left kidney of the sham-operated rats. Similar analysis at 20 weeks after clipping showed a fourfold increase in the left kidney and a 16-fold suppression in the right kidney compared with age-matched sham-operated control rats. The study demonstrates the profound changes that occur in renin gene expression in the clipped and contralateral kidneys in this model of hypertension and shows that these changes persist into the chronic phase of the hypertension.
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PMID:Kidney renin mRNA levels in the early and chronic phases of two-kidney, one clip hypertension in the rat. 264 44


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