Disease relevance of Hypertension, Renal

• Introduction to part II of the hypertension symposium. Prorenin, renal hypertension; diuretics and hyperlipidemia; angiotensin receptors and blocking drugs; a new treatment system [1].
• To determine the mechanism of blunted sympathetic reflex responses in early renovascular hypertension, we measured inotropic and chronotropic responses of the heart to beta-adrenergic stimulation in vivo and myocardial beta-adrenergic receptor number and adenylate cyclase activity in 10 dogs during an early stage of one-kidney renal hypertension [2].
• We produced cerebral aneurysms in 19 rats by unilaterally ligating the common carotid artery, inducing renal hypertension, and feeding beta-aminopropionitrile fumarate [3].
• To examine and characterize the vascular renin--angiotensin system in low-renin models of renal hypertension with and without the presence of overt renal insufficiency, we studied the formation and metabolism of angiotensin in isolated perfused rat hindquarter preparations [4].
• OBJECTIVES: We tested the hypothesis that a reduction in myocardial cyclic GMP would increase myocardial O2 consumption and that renal hypertension (One Kidney-One Clip, 1K1C)-induced cardiac hypertrophy would change this relationship [5].

Psychiatry related information on Hypertension, Renal

• Central action of acetylcholine on the behavior, pain threshold and duration of electrical convulsions in rats with renal hypertension [6].
• In addition, a series of manipulations ranging from mild water deprivation or ingestion of a dry meal to ether stress of rats with malignant renal hypertension was applied to examine the capacity of the RAS to generate angiotensin [7].

High impact information on Hypertension, Renal

• Reciprocation of renin dependency with sodium volume dependency in renal hypertension [8].
• Correction of renal hypertension in the rat by prolonged infusion of angiotensin inhibitors [9].
• The goal of the present study was to evaluate the role of endogenous endothelin-1 in renal hypertension in dogs [10].
• We investigated whether endothelial dysfunction might contribute to the exaggerated vasoconstriction that was induced by the administration of norepinephrine at the early stage of one-kidney, one-clip renal hypertension (1K1C) in rats [11].
• Thereby vasopressin may contribute to the development of malignant renal hypertension in rats [12].

Chemical compound and disease context of Hypertension, Renal

• Furthermore, in normal rats chronic beta-adrenergic blockade with propranolol caused no change in the development of the two-kidney renal hypertension [13].
• An infusion of saralasin sufficient to lower the blood pressure in five subjects with renal hypertension resulted in a rise in active renin concentration but no change in the concentration of inactive renin [14].
• Development and maintenance of renal hypertension in normal and guanethidine sympathectomized rats [13].
• Nitric oxide in essential and renal hypertension [15].
• Effect of captopril on renal hemodynamics in the treatment of resistant renal hypertension [16].

Biological context of Hypertension, Renal

• As PGI2 is a potent vasodilator, higher production by arteries during the 6-day period suggests that prostacyclin could play a modulator role on peripheral resistance during the initial phase of renal hypertension [17].
• The peak rate of rise of left ventricular pressure (dP/dt), the ratio of left ventricular dP/dt and the developed pressure during isovolumic contraction (dP/dt/P), myocardial oxygen consumption, and plasma norepinephrine levels increased after pinacidil administration in the sham-operated dogs, but did not change in the renal hypertension group [18].
• OBJECTIVE: To test the hypothesis that an angiotensin I converting enzyme inhibitor and a calcium channel blocker have different effects on the arterial baroreflex in renal hypertension [19].
• The influence of a 6-week treatment of female Wistar rats with one-kidney, one clip (1-K, 1 C) renal hypertension, with the calcium antagonist nifedipine on plasma volume, red cell Na+ handling and plasma atrial natriuretic peptide immunoreactivity (ANP-IR) was studied [20].
• We also examined the relationship between NPY gene expression and renin in two rat models of hypertension (two-kidney, one-clip renal hypertension (2K1C), and deoxycorticosterone-salt-induced hypertension (DOCA-salt)) characterized by a similar blood pressure elevation [21].

Anatomical context of Hypertension, Renal

• Rats with chronic renal hypertension were studied to determine whether the extracellular matrix proteins--collagen IV, laminin, and fibronectin--are increased in the thick-walled cerebral vessels in brain and those associated with areas of blood-brain barrier (BBB) breakdown to protein [22].
• To elucidate the role of the internal elastic lamina in the development of cerebral aneurysm, the bifurcation of the anterior cerebral artery and olfactory artery was histologically studied in control and experimental rats treated with unilateral carotid ligation and renal hypertension [23].
• The role played by the sympathetic nervous system in one-kidney renal hypertension was studied in animals in which the peripheral sympathetic nervous system was completely ablated by chronic guanethidine treatment and adrenal demedullation [24].
• Experimental renal hypertension and [3H]-noradrenaline release from the rabbit hypothalamus: enhanced K+-evoked overflow of tritium and lack of facilitation through presynaptic angiotensin II receptors [proceedings] [25].
• 1. To determine the possible role of arterial cyclic AMP in the pathogenesis of hypertensive vascular hypertrophy and hyperplasia, the changes in the level of this nucleotide were studied during the development of renal hypertension in rats with aortic ligation between the renal arteries [26].

Gene context of Hypertension, Renal

• There is more persuasive evidence for increased endothelin-1 activity in secondary forms of hypertension, including pre-eclampsia and renal hypertension [27].
• Plasma-levels of endothelin-1 and angiotensin-II and reactivity of arterial blood pressure to exogenous sympathomimetics and vasoactive peptides in rat model of malignant renal hypertension [28].
• Angiotensin II subtype 1 (AT1) receptor antagonists reduce mean arterial pressure in various experimental models of hypertension, including two-kidney, one clip (2K1C) renal hypertension [29].
• Vascular angiotensin converting enzyme in the development of renal hypertension [30].
• Plasma from persons with renal hypertension contained varying amounts of inactive renin but the mean percentage (35%) was lower than normal [14].

Analytical, diagnostic and therapeutic context of Hypertension, Renal

• Segmental renin sampling and partial nephrectomy in renal hypertension [31].
• 1. The effect of chronic administration of propranolol on the development and maintenance of severe renal hypertension in rats subjected to unilateral renal artery constriction was studied in relation to possible changes in peripheral PRA and the blood and tissue levels of propranolol [32].
• However, in contrast to their possible renoprotective effect in diabetic nephropathy or in renal hypertension, there are increasing evidence that, in the presence of a reduction in renal perfusion, intrarenal haemodynamic effect of ACEi may lead to compromised renal function [33].
• Effect of castration on the experimental renal hypertension of the rat. Blood pressure, nephrosclerosis, long-chain fatty acids, and N-acetylation of PAH in the kidney [34].
• Intravenous injection of Hoe 892 induced a dose dependent decrease of systemic BP in anesthetized rats (ED25 of 2.2 micrograms/kg) and in the rats with acute renal hypertension [35].

References