Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The arteriolar lesions of rats with deoxycorticosterone (DOCA)-salt hypertension have been studied by colloidal carbon injection and light- and electron-microscopy. 2. Colloidal carbon particles enter the media of arterioles to form focal deposits when hypertension develops. 3. The focal lesions are similar to those seen after angiotensin infusion or renal artery constriction. They are characterized by endothelial damage and plasma deposition in the media. 4. Heavy deposition of carbon in the glomeruli of DOCA-treated animals was found to be caused by increased mesangial uptake and not by hypertensive vascular damage. 5. Angiotensin II concentrations fell during the development of hypertension and vascular lesions. The renin-angiotensin system was not implicated in the development of vascular damage in this form of hypertension.
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PMID:The arteriolar lesions of steroid hypertension in rats. 107 33

The responses of blood pressure, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) to infusion of either angiotensin II (10 ng/Kg/min) or norepinephrine (100 ng/Kg/min) were observed in 25 patients with essential hypertension. The difference in modes of response between low renin essential hypertension and normal or high renin essential hypertension was analyzed. For comparison, 5 patients with Conn's syndrome, 4 with renovascular hypertension, and 5 normotensive subjects were also studied. Following infusion of antiotensin II the changes in diastolic blood pressure (DBP) were +24+/-3.0 mmHg in low renin essential hypertension and +25+/-3.1 mmHg in normal or high renin essential hypertension in PRA -0.28+/-0.06 ng/ml/h in low renin essential hypertension and -0.69+/-0.02 mg/ml/h in order and in PAC +3.7+/-1.4 and +7.6+/-1.8 ng/100 ml respectively. There was a significant difference in magnitude of response in PRA between the 2 groups of essential hypertension (p less than 0.05). Norepinephrine induced rise in DBP with decreases both in PRA and PAC. The mean changes in DPB were +6+/-1.4 mmHg in low renin essential hypertension and +16+/-2.2 mmHg in another and the pressor response in the later was significantly greater (p less than 0.01). The changes in PRA were -0.14+/-0.07 ng/ml/h in low renin essential hypertension and -0.67+/-0.26 ng/ml/h in normal or high renin essential hypertension, and in PAC -4.9+/-1.3 and -3.3+/-1.9 ng/100 ml respectively. The greater fall in PRA in normal or high renin essential hypertension was observed but the difference between the 2 groups of essential hypertension was not significant. The changes in PAC did not parallel the changes in PRA. Angiotensin II indcued essentially similar effects on blood pressure in both groups but the greater feedback inhibition of PRA was produced by this peptide in normal or high renin essential hypertension than in low renin essential hypertension. Norepinephrine induced significantly greater pressor effect in normal or high renin essential hypertension. The adopted dose of norepinephrine suppressed both PRA and PAC and a tendency to the greater fall in PRA was observed in normal or high renin essential hypertension. There was no difference in responses of PAC to both agents between the 2 groups of essential hypertension.
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PMID:Effect of pressor agents on blood pressure, plasma renin activity and plasma aldosterone concentration in essential hypertension. 115 95

The plasma renin activity in both peripheral venous blood and the renal vein of the involved kidney showed high values. Angiotensin infusion elevated the urine volume and angiotensin excretion on the intact side, and the difference in urine volume and angiotensin excretion between the two sides was accentuated after angiotensin infusion. These findings are useful for the diagnosis of the stenotic side in renovascular hypertension. No difference in the prognosis of extirpation of the involved kidney and of vascular reconstruction of the stenotic artery was found for the treatment of renovascular hypertension. However, autotransplantation of the involved kidney was found to be more useful, since it allowed improvement of renal circulation, suppression of thrombosis formation, and the maintenance of kidney tissue.
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PMID:Diagnostic value of plasma renin activity and plasma angiotensin II in renovascular hypertension. 115 43

Hypertension in endocrine disorders (Cushing's syndrome, Conn's syndrome, Pheochromocytoma) is frequently accompanied by a confusing clinical symptomatology. The underlying pathology is a cortical hyperplasia or a tumor of the adrenal cortex or medulla. The differentiation from other causes of hypertension is primarily based upon laboratory findings (plasma and urinary concentration of cortico-steroids, Renin, Angiotensin and catecholamines as well as their derivates). The preoperative tumor localization by urography, arteriography and adrenal venography as well as the visualization of glandular hypertrophy by adrenal venography is of fundamental importance with regard to treatment of these disorders.
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PMID:[Radiology of suprarenal glands (author's transl)]. 117 39

To explore the molecular and subcellular effects of Angiotensin II during the early phase of an experimental hypertension, biochemical and morphological changes induced by continued administration of subpressoric Angiotensin II doses were traced in rats. After the treatment, the endogenous noradrenalin and dopamine content was changed in various brain regions, the turnover rate of noradrenalin was lowered, and the neuronal 3H noradrenalin uptake was delayed and reduced. Electron microscopy revealed an increase in number and granulation of adrenergic vesicles in the hypothalamus, and characteristic changes at pre- and postsynaptic membrane complexes. The interaction between central effects of angiotensin II and the adrenergic system presumably involves disturbance at the level of neuronal membranes.
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PMID:[The mechanism of action of peptides acting on smooth muscle. II. Relationships between angiotensin II and adrenergic systems with reference to blood pressure regulation]. 118 40

The effect of one single dose of 10 ng Angiotensin II/kg body weight upon affirmed conditional-reflectory response patterns (two-dimensional conditional-reflectory decision process and periodicities of conditional-reflectory processes) was studied in 50 male albino rats in which a neutrotically induced hypertensive blood pressure regulation had been elicited by stress exposure for 135 days. Contrary to healthy animals in which Angiotensin II was demonstrated to act in a biphasic manner, the neurotic animals revealed a monophasic action manifesting itself by a generalized centralnervous excitation. It was noticed, furthermore, that the information processing and regulatory processes of the CNS are considerably disturbed. The chronically hypertensive systolic blood pressure values of neurotic animals, like in healthy ones, show a brief, transient rise immediately following administration of Angiotensin II. These results are not only another proof of a neurotropic component of Angiotensin II action, but they show also that this action allows one to judge the state of disturbed nervous functions. The correlation of the neurotropic effect of Angiotensin II with pathogenetic mechanisms of experimental neurotically induced hypertension is discussed.
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PMID:[Effect of angiotensin II on the conditional relfex response patterns of neurotic albino rats]. 124 Dec 19

We measured arterial plasma angiotensin II concentration, renal blood flow, and arterial blood pressure in six conscious dogs during intravenous infusion of angiotensin II (5, 10, and 20 ng/kg per min). The same measurements were made on a different occasion in the same six animals, while they were conscious, before and during constriction of a main renal artery. Arterial blood pressure and plasma angiotensin II rose and renal blood flow decreased in both experiments. The similarity of regressions for plasma angiotensin II concentration and arterial blood pressure in the two experiments strongly suggests that the rise of circulating angiotensin II after renal artery constriction is sufficient to account for the hypertension by its direct pressor action. As discussed, a different mechanism seems likely to be involved in the later stages of renal hypertension. Angiotensin II is more likely to be in the 5-isoleucine form than in the 5-valine form in the dog. In contrast to the rat, plasma concentrations of the heptapeptide (angiotensin III), hexapeptide, and pentapeptide fragments of angiotensin II are low in the dog.
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PMID:Blood pressure and plasma angiotensin II concentration after renal artery constriction and angiotensin infusion in the dog. (5-Isoleucine)angiotensin II and its breakdown fragments in dog blood. 126 Sep 74

Left ventricular hypertrophy is an important risk factor for sudden death and other cardiovascular morbidity and mortality irrespective of the level of arterial blood pressure. Left ventricular hypertrophy, i.e. an increase in wall thickness at the expense of left ventricular volume, is an adaptive mechanism observed in patients with long standing arterial hypertension. Severe left ventricular hypertrophy is associated with a reduction in left ventricular compliance, impaired coronary reserve, ventricular ectopy, and impaired contractile function. Left ventricular hypertrophy can be reduced by antihypertensive therapy; however, not all antihypertensive agents have the same effect on left ventricular hypertrophy despite their similar effects on arterial blood pressure. Angiotensin converting enzyme (ACE) inhibitors appear to be the most powerful agents for reducing left ventricular hypertrophy, followed by the nondihydropyridine calcium antagonists. In addition to reducing left ventricular mass and arterial blood pressure, certain calcium antagonists also improve left ventricular filling, suppress ventricular ectopy, and maintain or enhance contractile function. However, despite these beneficial effects, it is not known whether the risk of cardiovascular morbidity and mortality can be prevented or reduced by specific antihypertensive agents.
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PMID:Does a reduction in left ventricular hypertrophy reduce cardiovascular morbidity and mortality? 128 78

Angiotensin converting enzyme inhibitors are now widely used in the treatment of hypertension and heart failure. They are clearly as effective as other conventional antihypertensive agents in reducing blood pressure and combined with diuretics seem likely to transform current management of chronic heart failure. Myocardial infarction remains the major cause of death in patients with raised blood pressure and current studies should establish whether the attractive features of ACE inhibitors translate into reduction in the rate of infarction or its consequences. Similarly, whilst symptomatic benefit undoubtedly accrues from their use in heart failure it is less clear that they can prolong life particularly when used in the immediate setting of a myocardial infarction. Again a number of ongoing major trials are set to establish whether these drugs reduce death in patients with chronic heart failure (V-HeFT II, SOLVD) and in patients immediately after myocardial infarction (CONSENSUS II, SAVE,. AIRE, GISSI III and ISIS IV). The physician has a wide choice of ACE inhibitors with different pharmacological profiles for clinical use.
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PMID:Cardioprotection and ACE inhibitors. 130 64

Angiotensin II (Ang II) inhibits renin secretion and production from the kidney, but the effect of Ang II on adrenal renin is not clear. Nephrectomy, via elevated plasma adrenocorticotropic hormone (ACTH) and potassium, is a strong stimulator of adrenal renin production in the rat. This stimulation is inhibited by the infusion of Ang II, suggesting a negative feedback between Ang II and adrenal renin. In the present study, we examined the effect of Ang II on adrenal renin using a primary culture of rat glomerulosa cells. Cells were exposed to ACTH (10(-11) M), high potassium (8 and 12 mM), db-cyclic AMP (db-cAMP), (10(-3) M), or Ang II (10(-11) to 10(-5) M) for 24 hours, and active renin and inactive renin were measured. Active renin was predominant in the cells, whereas inactive renin predominated in the medium. Ang II stimulated renin production in a dose-dependent fashion (cell-active renin, 1.21 +/- 0.20 to 2.39 +/- 0.16; medium-inactive renin, 2.59 +/- 0.40 to 6.14 +/- 0.49 ng Ang I/10(6) cells). Both ACTH and db-cAMP significantly stimulated active renin in the cells (ACTH, 1.73 +/- 0.14 to 9.44 +/- 0.98; db-cAMP, 1.45 +/- 0.16 to 3.96 +/- 0.71 ng Ang I/10(6) cells) and inactive renin in the medium (ACTH, 4.98 +/- 0.38 to 43.7 +/- 5.63; db-cAMP, 3.80 +/- 0.32 to 33.55 +/- 5.62 ng Ang I/10(6) cells). The addition of Ang II (10(-7) M) blunted the stimulation of renin production by both ACTH and db-cAMP by 60%. High potassium-stimulated renin production was not inhibited by Ang II.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Mar
PMID:Effect of angiotensin II on renin production by rat adrenal glomerulosa cells in culture. 131 12


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