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

The role of renin-angiotensin system has been examined in the maintenance of hypertension in acute and chronic two-kidney (36 weeks) and chronic one-kidney (12 weeks) Goldblatt hypertensive rats using three inhibitors of this system. The inhibitors used were URI-73A, a synthetic analog of lysophosphatidylethanolamine, which inhibits renin both in vivo and in vitro, SQ14,225, a potent converting enzyme inhibitor, and [Sar1, Thr8] angiotensin II, an angiotensin II antagonist. When the inhibitors were administered in acute (high renin) hypertensive rats, they all lowered blood pressure significantly. However, in the chronic (low renin) hypertensive phase, both renin and converting enzyme inhibitors lowered blood pressure, whereas, Sar1, Thr8 failed to lower blood pressure. The renin inhibitor lowered plasma renin activity (PRA), and SQ14,225 and [Sar1, Thr8] Ang II increased PRA. Further studies on water and electrolyte balance with one-kidney model hypertensive and uninephrectomized control rats showed no change in plasma volume. However, there was increased 24-hour urinary output and increased sodium excretion. This study indicates that in chronic renal hypertensive rats, blood pressure reduction is possible by either renin on converting enzyme inhibitor, but not by angiotensin antagonists. Since volume did not change either during the development or reversal of hypertension, volume did not appear to play a major role in the maintenance of hypertension.
Hypertension
PMID:Role of renin-angiotensin system in chronic renal hypertensive rats. 23 87

Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin-angiotensin system is responsible for the initiation of renovascular hypertension in the one-kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.
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PMID:Inhibition of angiotensin conversion and prevention of renal hypertension. 23 18

1. Aorta homogenate contains renin-like activity which on incubation generates angiotensin I over a wide pH range. 2. Rat aortic renin measured at an incubation pH of 6.5 rose and fell in parallel to plasma renin with salt depletion and salt-loading respectively. Renin little relationship with plasma renin. 3. Aortic renin (pH 6.5) was elevated in Goldblatt-two kidney hypertension and slowly fell for 24h after bilateral nephrectomy whereas the fall in plasma renin was complete by the first hour. Aortic renin (pH 5.3) was also high, but did not fall after bilateral nephrectomy. 4. Aortic renin (pH 6.5) is probably derived from plasma renin whereas renin measured at pH 5.3 is probably a tissue renin. 5. The prolonged half-life of aortic renin (pH 6.5) explains the observation that the renin-angiotensin system appears to be active in maintaining blood pressure for several hours after bilateral nephrectomy whereas the decline in plasma renin is rapid and does not continue significantly beyond 1 h.
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PMID:Role of persistent vascular renin after bilateral nephrectomy in Goldblatt-two kidney hypertension. 28 58

We measured indices of the renin-aldosterone system and body-fluid spaces in 11 adolescents who had received a renal transplant after removal of their own diseased kidneys. None had hypervolemia but 6 had hypertension. Renal angiography revealed greater than 50% luminal occlusion by allograft renal-artery stenosis (RAS) in only the 3 patients who had severe hypertension refractory to conventional medical therapy. Excessive peripheral plasma renin activity (PRA) distinguished these patients from those who had less severe stenosis or normal angiogram, and diuretic stimulation heightened the PRA differences. We conclude that significant allograft RAS does not necessarily act like a typical single-kidney Goldblatt model until after volume depletion. Our findings indicate that peripheral PRA values can be used to assess the degree of graft ischemia clinically. This permits early identification of patients who have severe RAS that probably will be difficult to control medically, and, therefore, should be followed closely with a view of reconstructive vascular surgery before further deterioration of renal function.
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PMID:Allograft renal-artery stenosis: increased peripheral plasma renin activity as an early indicator of uncontrollable hypertension. 36 8

The synthesis and deposition of collagen and other proteins has been measured in the aorta of the rat by radiolabeling in short term organ culture. Under these conditions, the synthesis of collagen and other proteins is linear for at least five hours. Autoradiography demonstrates a labeling in all cell layers and protein deposition in the extracellular matrix. Hypertension was induced by renal ischemia using Goldblatt's technique. The synthesis and deposition of collagen was stimulated in aorta from the first week of hypertension and in pregnancy, and was even more increased in hypertensive pregnant animals. Reserpine suppresses the rise in blood pressure in operated animals and prevents these modifications.
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PMID:Aortic collagen biosynthesis during renal hypertension, pregnancy and hypertension during pregnancy in the rat. 36 58

1. The pressor response to angiotensin II was reduced in rats with early (less than 6 weeks) and chronic (greater than 4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA-salt hypertension. 2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness. 3. After bilateral nephrectomy the pressor responses to angiotensin were similar. 4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.
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PMID:Pressor responsiveness to angiotensin in renovascular and steroid hypertension. 39 91

Two-kidney, one clip Goldblatt rats were treated with oral converting enzyme inhibitor captopril (SQ14,225) 6 mg/kg/day for 3 weeks after they had developed hypertension. Before treatment, systolic blood pressure rose from 143 to 202 mm Hg (p less than 0.05). Tail vein infusions of saralasin 10 microgram/kg/min in conscious rats reduced systolic blood pressure from 202 to 121 mm Hg (p less than 0.05) at 8 weeks after clipping the renal artery and before treatment with captopril. Chronic treatment with captopril for 3 additional weeks lowered blood pressure to 173 mm Hg (p less than 0.05). When saralasin infusion was repeated during treatment with captopril, blood pressure fell from 173 to 159 mm Hg (p less than 0.05). Blood pressure rose to 197 mm Hg within 4 days after captopril was discontinued and saralasin infusion 3 weeks after captopril (15 weeks after clipping the renal artery) again resulted in a dramatic fall in blood pressure from 197 to 142 mm Hg (p less than 0.05). Goldblatt rats who had not received captopril showed no blood pressure response to saralasin infusion at 12 weeks after renal artery clipping. The present study demonstrates that partial inhibition of the renin-angiotensin system with captopril results in a delay in the natural evolution of clip hypertension retarding the appearance of hypertension that is resistant to acute saralasin infusion.
Hypertension
PMID:Prolongation of the saralasin responsive state of two-kidney, one clip Goldblatt hypertension in the rat by the orally administered converting enzyme inhibitor captopril (SQ14,225). 39 95

Renin was extracted and purified from human, dog, hog, rat, beef, rabbit and sheep kidneys. The renin "concentration" of these preparations was determined and expressed in international (Goldblatt) units by measuring the pressor effect produced by intravascular injection into normal dogs of a permanent colony. The renin "activity" was determined by bioassay, in the rat, of the angiotensin produced by incubation in vitro with renin substrate prepared from the serum of nephrectomized dogs. The rate of angiotensin formation was proportional to the concentration of renin, independent of the substrate concentration, and rather similar for renin of all seven species (mean rate = 55 x 10(4) ng angiotensin/unit renin/16 hrs). Due to this uniformity, either of the two international reference preparations of renin (human or hog) from the World Health Organization can serve as an internal standard in the assay of reninof each of the seven species, to express their concentration in terms of the international unit. Renin substrate from hog plasma was suitable for the assay of human, dog and hog renin (mean rate = 55 x 10(4)). However, it reacted much more slowly with the renin of rat, beef, rabbit and sheep (mean rate = 9 x 10(4)) and was, therefore, less suitable for their assay.
Hypertension
PMID:Micromethod for the assay of renin of seven species. 39 36

Changes of activity of the alkaline phosphatase are investigated in the border of the outer media of vessels in two different models of hypertension (Goldblatt and Carotis-Sinus) in the rat. After onset of hypertension an increase of activity takes place in an area largely overlapping a necrosis of the outer medial region of the aorta. The formation of regenerated tissue leads to a thickening of the adventitia and to a decrease of the activities. Changes of the activities in the peripheral vessels presumably are due to participation of other factors. Indications to this effect are discussed.
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PMID:[Changes of activity of alkaline phosphatase at the circulatory system in experimental hypertension of the rat (author's transl)]. 40 22

Tubular uptake of ferritin given intravenously was studied in the right and left kidneys of 74 Goldblatt-hypertensive rats. Previous observations pointed out the pathologically enhanced permeability of glomerular barrier as the cause of the phenomenon. It was assumed, that the extent of tubular areas taking up ferritin, refers to the number of damaged glomeruli. The process was characterized semiquantitatively by planimetric measurements and determination of the non-hemin iron concentration in the renal cortical tissue. A more frequent and extensive tubular ferritin-uptake (and glomerular damage) was bilaterally recorded in the kidneys of malignant hypertensive rats in comparison to the benign ones. The development of the phenomenon in the clamped kidneys, being defended from high blood pressure, suggests a humoral factor behind the enhanced glomerular permeability. Saline intake has a beneficial effect on the glomerular damage similar to the hypertensive angiopathy.
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PMID:Renal tubular ferritin-uptake, a consequence of the increased glomerular permeability, during the benign and malignant course of renal hypertension in rats. 42 54


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