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

The renin-angiotensin system has been implicated in the genesis of pre-eclampsia. To avoid fetal toxicity, five women were studied who developed hypertension, proteinuria, and edema in the last trimester of pregnancy and whose BP elevation persisted immediately postpartum. At about 6 hours after delivery the CE enzyme inhibitor (SQ 20,881) was given in incremental doses ranging from 0.25 to 3.0 mg. per kilogram intravenously, before and after diuresis with furosemide, 40 mg. intravenously. BP was measure every 2 minutes and PRA and angiotensin II concentration before treatment, 30 minutes after 0.25 to 0.30 mg. per kilogram, and 30 minutes after 2.0 to 3.0 mg. per kilogram. Echocardiographic assessment of CI and PVR was performed before treatment and after a maximum dose in three patients. Before diuresis, CE blockade had no effect on heart rate, BP, CI, PVR, or PRA, regardless of whether the patient was in positive or negative fluid balance or was sodium loaded or restricted over the preceding 24 hours. Angiotensin II fell by 77 and 10 per cent, respectively, after 0.25 mg. per kilogram was given to two patients, but rose slightly in the other three patients, then fell an average of 46 per cent after 1.0 to 3.0 mg. per kilogram were given. After diuresis, 1.0 mg. per kilogram resulted in a 24 per cent fall in BP which persisted for 3 hours in two patients and a 14 per cent fall which lasted for 30 minutes after 1.0 or 3.0 mg. per kilogram in a third patient. It is concluded that the BP elevation which persists after delivery in certain patients with pre-eclampsia is not angiotensin II dependent.
 ...
PMID:SQ 20,881: effect on eclamptic--pre-eclamptic women with postpartum hypertension. 68 62

Recently, the availability of a number of specific inhibitors of the renin-angiotensin system has made it possible to address certain critical questions concerning the role of angiotensin II in physiologic homeostasis and in a number of pathologic states. These studies indicate that angiotensin II does not have an obligatory role in blood pressure maintenance in the normal, sodium replete individual, but it is essential following sodium depletion. The role of angiotensin II in feedback control of renin secretion is confirmed as is its importance in aldosterone stimulation both in relation to posture and sodium depletion. Angiotensin II is responsible for the initial pressor response of experimental renovascular hypertension and appears to be important in the initiation of chronic renovascular hypertension. Converting enzyme blockers and competitive inhibitors of angiotensin II are helpful in the diagnosis of clinical renovascular hypertension and in the identification of renin dependent hypertensives. Homeostatic mechanisms leading to maintenance of blood pressure and accumulation of edema in experimental congestive heart failure appear to be dependent on angiotensin II.
 ...
PMID:George C. Griffith lecture. The role of renin in normal and pathological cardiovascular homeostasis. 79 34

Eighteen patients with advanced or malignant hypertension due to essential hypertension, systemic lupus erythematosus or chronic glomerulonephritis were infused intravenously with 1-Sar-8-Ile-Angiotensin II, a competitive antagonist of aniotensin II. The spectrum of responses was broad from a mild elevation to a marked fall in blood pressure. The changes in mean blood pressure caused by this peptide showed a significant correlation with the level of peripheral plasma renin activity immediately before the infusion (r=0.5652, p less than 0.02). This peptide infusion reduced blood pressre in 12 patients (responders), but not in 6 (non-respnders). There were no differences with age, sex and severity of hypertension except for the level of peripheral plasma renin activity between the two groups. Our retrospective study showed that in 12 responders propranolol reduced blood pressure to near the normal level, while in 6 non-responders furosemide induced similar depressor response. It is concluded that the vasodepressor effect of this peptide correlates with the levels of peripheral plasma renin activity and that the responses to this drug can be used as a guide for the selection of effective antihypertensive drugs.
 ...
PMID:Clinical evaluation of angiotensin II antagonist in advanced hypertension. 88 41

Patients with essential hypertension were sodium deprived by five days on a 10 mM sodium diet and were then infused with an incremental infusion of saralasin, a competitive inhibitor of angiotensin II. Patients with normal renin hypertension showed no change in lying or standing blood pressure during the infusion of saralasin. Angiotensin II is not, therefore, directly maintaining blood pressure in these patients when sodium deprived by diet, and is therefore unlikely to be playing any direct role in maintaining their blood pressure on their normal sodium intake. Patients with low renin hypertension showed a significant rise in blood pressure during saralasin infusion. Saralasin may be a further method of distinguishing low renin hypertensives from other hypertensives if they are infused when sodium deprived by diet.
 ...
PMID:Angiotensin II blockade in patients with essential hypertension. 107 4

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.
 ...
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.
 ...
PMID:Effect of pressor agents on blood pressure, plasma renin activity and plasma aldosterone concentration in essential hypertension. 115 95

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.
 ...
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.
 ...
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.
 ...
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

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


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>