Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypertensinogenic effects of 19-hydroxyandrostenedione (19-OH-A-dione), which we reported as an amplifier of the action of aldosterone on the basis of the results obtained in bioassays using adrenalectomized rats, were evaluated in intact rats with both adrenals and kidneys. The administration of 19-OH-A-dione to the rats caused sodium retention and the 19-OH-A-dione treated rats developed high blood pressure, suppressed plasma renin activity and low plasma aldosterone, corticosterone and deoxycorticosterone concentrations. The hypertensinogenic potency of 19-OH-A-dione was incomparably higher than that of DOCA. The results indicate that 19-OH-A-dione is a potent hypertensinogenic steroid and causes the hypertensive state similar to mineralocorticoid excess. The evaluation of 19-OH-A-dione concentrations in human plasma revealed that 19-OH-A-dione is present in human peripheral circulation. It appears to be secreted by the adrenal cortex under the control of ACTH and the renin-angiotensin system. Plasma 19-OH-A-dione concentrations in patients with normal renin essential hypertension and low renin essential hypertension are higher than those in control subjects. 19-OH-A-dione is a newly recognised hypertensinogenic steroid in man.
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PMID:19-Hydroxyandrostenedione: a potent hypertensinogenic steroid in man. 631 Feb 35

To determine the contribution of receptor number and affinity to changes in vascular reactivity to angiotensin II (AII) in hypertensive rats, we have investigated the binding of 125I-AII to a particulate fraction of the rat mesenteric artery of hypertensive rats. In two-kidney, one clip hypertensive rats, receptor concentration (Bmax) was 83 +/- 13 fmol/mg and the dissociation constant (Kd) 0.6 +/- 0.1 nM vs 75 +/- 5.3 fmol/mg and 0.6 +/- 0.1 nM in normotensive controls, although PRA was much higher in the former. Bmax was reduced in these hypertensive rats after sodium depletion, as in normal rats. One-kidney, one clip hypertensive rats (Bmax 88 +/- 17 fmol/mg, Kd 0.6 +/- 0.1 nM) did not differ from uninephrectomized control rats (96 +/- 9 fmol/mg, Kd 0.5 +/- 0.1 nM). In DOCA-salt hypertensive rats, binding capacity was increased (125 +/- 2 fmol/mg, Kd 0.7 +/- 0.0 nM) vs uninephrectomized salt-loaded rats (Bmax 95 +/- 6 fmol/mg, Kd 0.6 +/- 0.1 nM), although PRA was suppressed comparably in both groups. The salt-loaded rats did not differ from uninephrectomized controls drinking water. We conclude that changes in the circulating renin-angiotensin system do not explain all the variations in receptor number in hypertensive rats. Our results suggest a role of mineralocorticoids in the regulation of vascular AII receptors.
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PMID:Vascular angiotensin II receptors in renal and DOCA-salt hypertensive rats. 631 55

The effect on blood pressure and heart rate, following administration of the same intracerebroventricular (ivt) and intravenous (iv) doses of captopril, was compared in freely moving DOCA-salt hypertensive rats, with chronically implanted ivt, iv and intraarterial cannulae. Ivt captopril (500 micrograms) in DOCA-salt rats showed an initial pressor response followed by a long lasting hypotensive effect. The ivt effect was greater than that following iv administration. No effect was observed in normotensive controls either ivt or iv. ASA or naloxone pretreatments significantly lowered the captopril hypotensive effect, thus suggesting an involvement of prostaglandin and opioid systems in blood pressure elevation in "non renin dependent" hypertension.
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PMID:Cardiovascular responses of conscious DOCA-salt hypertensive rats to acute intracerebroventricular and intravenous administration of captopril. 634 5

The purpose of this review is to focus on alterations in vascular muscle membrane potentials (Em), ionic permeabilities, and ionic transport systems which may either contribute to or be a consequence of the hypertensive state. Three models of hypertension are discussed: 1) deoxycorticosterone-salt (DOCA-salt)-induced hypertension; 2) low-renin (presumably volume expanded) renal hypertension (LRRH); and 3) the spontaneously hypertensive rat (SHR) of the Okamoto-Aoki Kyoto-Wistar strain and its normotensive genetic control (WKY). The importance of studying all possible mechanisms of increased contraction in vascular smooth muscle is stressed.
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PMID:Membrane mechanisms in arterial hypertension. 634 56

Efferent renal innervation is composed of postganglionic sympathetic fibers to the renal arterioles, juxtaglomerular apparatus, and renal tubules. Increased efferent renal sympathetic nerve activity results in increased renal vascular resistance, renin release, and sodium retention. These responses from enhanced renal sympathetic activity contribute to normal cardiovascular homeostasis but could also 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 DOCA-salt-treated rat, suggesting that these responses are due, at least in part, to loss of efferent renal nerve activity. Similar sympathetically mediated renal vasoconstriction has been implicated in the pathogenesis of early essential hypertension in man. Recent studies indicate that the kidney is a sensory organ with mechano-receptive and chemoreceptive afferent renal nerves involved in renorenal and cardiovascular regulation. 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 due to change in renin activity or sodium excretion but is associated with decreased activity of the sympathetic nervous system. These findings suggest that the afferent renal nerves contribute to the pathogenesis of renovascular hypertension by enhancing the activity of the sympathetic nervous system. The role of the afferent renal nerves in renovascular hypertension in humans warrants further study.
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PMID:Renal nerves in the pathogenesis of hypertension in experimental animals and humans. 634 99

A possible role for vasopressin in the development and/or maintenance of DOCA hypertension in pigs was studied. In control pigs mean arterial blood pressure (MABP), plasma lysine vasopressin (LVP) concentration, the 24-h urinary excretion of LVP (ULVPV) and plasma renin activity (PRA) did not change throughout the 30 days of the experiment. In DOCA-treated pigs MABP began to increase from the initial level of 95 +/- 2 mm Hg within 5 days and reached a level of 127 +/- 3 mm Hg between days 20-30 (P less than 0.01). At this time in the DOCA treated pigs, ULVPV increased threefold (P less than 0.05), although PLVP was unchanged and PRA was reduced to almost zero. After 30 days the pigs were fed a low sodium diet. This was without effect on MABP, PLVP and ULVPV in control pigs. However, in the DOCA-treated pigs, MABP fell from 133 +/- 2 to 112 +/- 6 mm Hg, accompanied by a 60% fall in ULVPV. PLVP was unchanged. Thus in DOCA-treated pigs, LVP appears not to be involved in the development of hypertension, but may be involved in its maintenance.
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PMID:Increased urinary vasopressin excretion in the DOCA-hypertensive pig. 636 64

An infant with urinary sodium wasting is described. The plasma renin activity and plasma aldosterone concentration were distinctly raised. Administering DOCA was without effect. The condition pseudohypoaldosteronism is due to renal tubular unresponsiveness to endogenous aldosterone and can be adequately treated by salt replacement.
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PMID:[Pseudohypoaldosteronism: a special form of sodium loss in infancy]. 639 25

The case of a two month-old child admitted because of dystrophy is presented. At physical examination she presented a growth retardation (-2DS) as well as cutaneous and mucosal pallor. Metabolic acidosis, hyponatremia, hyperkaliemia and salt loss were demonstrated. Aldosterone, both plasmatic and urinary, was increased. Plasma renin activity, was also increased. In respect to renal function, hypercalciuria was found but not other abnormalities neither in the renal nor suprarrenal function were noticed. The electrolytic levels in sweat, saliva and feces were also normal. The clinical and laboratory findings were not modified with the DOCA test. Spirolactone caused an increase in salt loss. Treatment with indometacine improved both the clinical and analytical findings. On the other hand, treatment with chloride sodium (4 gr p.o. per day) also improved dramatically the disturbances. In the last 12 months she has growth up normally. At the same time, the renal loss of sodium has decreased and aldosterone, both plasmatic and urinary, is not so increased as it was at diagnosis. Finally, electrolytic parameters are fully normal.
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PMID:[Review of pseudohypoaldosteronism. Apropos of a clinical case in a 2-month-old girl]. 639 46

The development of hypertension in two-kidney, one clip renal hypertensive rats (2K, 1C RHR) was not altered by treatment with DOCA and saline solution as drinking fluid for two months of observation. However, the administration of DOCA and salt suppressed plasma renin activity (PRA), the renal renin content (RRC) of the clipped kidney and the response to a single oral dose of captopril (10 mg/kg). The weight of the contralateral kidney was increased by the administration of DOCA-salt, while that of the ischaemic kidney was not changed. The withdrawal of DOCA-salt treatment restored the PRA and the effects of captopril to a similar degree to the non-treated group. The acute hypotensive effects of captopril were reduced on the 10th week compared with the 7th week after renal arterial constriction in 2K, 1C RHR. The fall in blood pressure induced by captopril significantly correlated with the initial PRA both in the 7th and 10th week after clipping. There was a significant correlation between PRA and RRC of the clipped kidney. Rats previously treated with DOC-salt had either removal of the contralateral kidney with removal of the clip from the ischaemic kidney, or removal of the ischaemic kidney. Blood pressure fell to normal levels in the unclipped group and in the nephrectomy group, but the fall in the latter group was transient and within two weeks had risen to significantly higher levels than in the unclipped group. It is concluded that structural vascular change following DOC-salt hypertension is insufficient to cause persisting hypertension except when it occurs in the renal circulation.
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PMID:Effect of DOCA-salt on angiotensin dependency and surgical reversal of hypertension in two-kidney, one clip renal hypertensive rats. 639 14

A model of hypertension induced by mineralocoriticoid-excess in the sheep is described. Deoxycorticosterone acetate (DOCA), 100 mg/kg was implanted subcutaneously in adult sheep (n = 13). Before DOCA administration, and for 30 days thereafter, mean arterial blood pressure (MAP), plasma electrolyte levels, plasma renin activities, water and electrolyte intakes and urinary outputs were monitored. Within 72 h after DOCA implantation MAP had risen from a control value of 83.0 +/- 2.0 to 93.0 to 3.0 mmHg, MAP stabilized at 114.0 +/- 3.0 mmHg three weeks later. Water intake had increased significantly by the 4th post-implant day and reached a maximum of 10.0 +/- 1.2 l/day by the third week. The following biochemical changes were significant within 24 h after DOCA implantation; (1) plasma potassium fell from 4.4 +/- 0.1 to 3.42 +/- 0.13 mEq/l; (2) plasma sodium rose from 144.4 +/- 0.6 to 147.0 +/- 0.4 mEq/l; (3) plasma renin activity fell from 1.29 +/- 0.42 to 0.13 +/- 0.08 ng ANG l/ml/h. The rapidity of onset and reversal of arterial pressure elevation in this model render it a useful tool in providing insight into the mechanism responsible for this form of hypertension.
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PMID:Deoxycorticosterone acetate hypertension in the sheep. 639 38


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