Disease relevance of REN

• In untreated animals, coronary occlusion produced significant increases in renin activity and arterial and venous levels of angiotensin I and angiotensin II [1].
• Myocardial ischemia in benazeprilat-treated dogs increased plasma renin activity and circulating levels of angiotensin I [1].
• These studies suggest that the [99mTc]DTPA renal flow study coupled with captopril challenge may unmask intrarenal angiotensin II-dependent functional and hemodynamic changes of the stenotic kidney, and offers promise in the detection of renin-dependent hypertension [2].
• OBJECTIVE: To compare the effects of angiotensin converting enzyme inhibition (ACEI) (captopril 1 mg/kg i.v.) to direct renin inhibition (CP80794 3 mg/kg i.v.) on left ventricular and systemic hemodynamics and peripheral blood flows in advanced congestive heart failure (CHF) [3].
• CV-3317 (30 mg/kg) induced a slight hypotension (5 to 10 mmHg) in normotensive rats, but had no effect on the blood pressure of 1-kidney, 1 clip hypertensive rats and on that of a low renin type of DOCA/salt hypertensive rat [4].

Psychiatry related information on REN

• Angiotensin II, the final product of the prohormone-to-hormone conversion reaction mediated by renin and angiotensin converting enzyme, was found to exist in the same cell as renin by immunohistochemical studies of brain sections and with cloned and cultured neuroblastoma cells [5].
• These data indicate that elevations in the plasma vasopressin concentration within the range observed during 24 h of water deprivation and nonhypotensive hemorrhage produced significant decreases in renin secretion and heart rate and elevations in blood pressure and corticosteroid secretion [6].
• The effects of 24 h of sleep deprivation and changes in plasma levels of renin and atrial natriuretic peptide were assessed [7].

High impact information on REN

• Effect of prostaglandin synthesis on renal function and renin in the dog [8].
• The antiserum did not affect blood pressure in sodium-replete dogs but decreased plasma renin activity and blood pressure in sodium-depleted animals [9].
• Renin-specific antibody for study of cardiovascular homeostasis [9].
• The antiserum also reduced blood pressure to control levels concomitant with suppression of plasma renin activity in uninephrectomized dogs with acute renovascular hypertension [9].
• As such, this system may be involved in the normal regulation of renal blood flow and renin release [10].

Chemical compound and disease context of REN

• L-163,017 also significantly reduces blood pressure in a renin-dependent model of hypertension, similar to an angiotensin converting enzyme inhibitor (Enalapril) and an angiotensin AT1 receptor-selective antagonist (L-159,282) [11].
• The groups were analyzed with consideration for body weight, hematologic values, hemodynamic parameters, and renal function (plasma renin activity, urinary debt, creatinine clearance, and sodium-excretory fraction) [12].
• As with other ACE inhibitors, quinapril had virtually no effect on the development of hypertension in the renin-independent one-kidney deoxycorticosterone (DOCA)-salt hypertensive rat [13].
• Plasma renin activity and angiotensin II immunoreactivity increased during hypoxia, and subsequent measurements were consistent with effective angiotensin-converting enzyme inhibition after administration of enalaprilat, and with angiotensin receptor blockade after administration of candesartan [14].
• Constriction of the pulmonary artery or thoracic inferior vena cava was maintained for 2 wk while daily measurements were made of plasma renin activity, plasma aldosterone, plasma volume, hematocrit, serum sodium and potassium concentrations, sodium and water balance, body weight, and arterial, caval, and atrial pressures [15].

Biological context of REN

• AngII significantly increased mean arterial blood pressure (+14 +/- 4 mmHg) and plasma aldosterone by 79% (+149 +/- 17 pg mL(-1)) and reduced plasma renin activity and sodium excretion (-41 +/- 16 mIU L(-1) and -46 +/- 6 mumol min(-1) respectively) [16].
• Long-term nitroglycerin infusion is associated with increases in plasma renin activity and catecholamine release rates, both of which may lead to excess angiotensin II and alpha-adrenergic-mediated vasoconstriction, particularly on withdrawal of nitroglycerin [17].
• However, CP80794 caused significantly greater increases in renal blood flow and suppressed renin activity to a greater degree than captopril [3].
• In two-kidney, one-clip (renin-dependent) hypertension, captopril (1.5 mg/kg bolus with 1.5 mg/min infusion) reduced mean arterial pressure (MAP) and ipsilateral glomerular filtration rate (GFR) without changes in the contralateral kidney [2].
• Effects of SQ 14,225, an orally active inhibitor of angiotensin-converting enzyme on blood pressure, heart rate and plasma renin activity of conscious normotensive dogs [18].

Anatomical context of REN

• In control dogs and those made hypertensive for 1 and 8 months by partially occluding a renal artery, contractile responses of mesenteric artery strips to adrenergic nerve stimulation and to norepinephrine, plasma renin activity and vascular angiotensin converting enzyme (ACE) activity were compared [19].
• Plasma renin activity in the blood obtained from a femoral artery and a renal vein was measured by use of radioimmunoassay [20].
• Placement of the constrictor on the left renal artery resulted in a significant increase in plasma renin activity which was accompanied by a significant hypertension (blood pressure greater than 140 mmHg) [21].
• An interaction of enalaprilic acid with the sympathetic nervous system was evaluated in dogs in which adrenergic activity was enhanced as a result of diuretic-induced renin release [22].
• The concentrations of immunoreactive angiotensin I (IR-Angiotensin I), plasma renin activity and angiotensin converting enzyme activity remained unaltered in the presence of coronary artery occlusion [23].

Associations of REN with chemical compounds

• Using specific competitive PCR assays, we found that RVHF was associated with significant increases in RV mRNA levels of angiotensin converting enzyme and angiotensin II type 2 receptor, and with significant decreases of RV expression of chymase and the angiotensin II type 1 receptor, while RV angiotensinogen and renin remained unchanged [24].
• Nitroglycerin infusion also was accompanied by a transient increase in plasma renin activity [17].
• Although captopril increased the secretion of active renin into renal venous plasma by six-fold, the secretion of total renin was unchanged because of a reciprocal fall in the secretion of inactive renin [25].
• The effects of enalaprilat (MK-422), an angiotensin converting enzyme inhibitor, were compared to those of SCRIP, a renin inhibitor, in experimentally induced left ventricular failure [26].
• While renin is a highly specific protease, converting enzyme has at least two principal substrates, angiotensin I and bradykinin [27].

Regulatory relationships of REN

• Hence, glucagon stimulates both PGE2 and renin release [28].
• The renal prostacyclin synthesis was augmented by endothelin without stimulating the renal renin release or norepinephrine output [29].
• In an in vitro study, the addition of somatostatin in doses of 0.01 and 0.05 microgram suppressed the renin release in dog renal cortical cell suspension by 74.3% and 53.6%, respectively [30].

Other interactions of REN

• OMA alone did not increase plasma renin activity and aldosterone, but resulted in a sustained increase in plasma adrenomedullin, with higher urinary atrial natriuretic peptide, adrenomedullin, and cGMP excretions than with ACEI+D [31].
• Endothelin-1 infusion also produced an inhibitory effect on renin release [32].
• COX-2 inhibition reduced urinary prostaglandin E(2) excretion in both groups but did not modify plasma renin activity in dogs with low (8.1+/-1.1 ng angiotensin I. mL(-1). h(-1)) or normal (1.8+/-0.4 ng angiotensin I. mL(-1). h(-1)) sodium intake [33].
• Effect of parathyroid hormone on renin secretion [34].
• Effect of glucagon on renin secretion in the dog [35].

Analytical, diagnostic and therapeutic context of REN

• During the micropuncture measurements, renal arterial pressure was reduced to range of 85 to 90 mm Hg in order to maximize renin secretion and intrarenal formation of angiotensin II [36].
• (ii) As (i), but additional servocontrolled reduction of the renal perfusion pressure (rRPP) to stimulate renin secretion and the formation of angiotensin II and aldosterone [37].
• The antihypertensive action of SCH 31846 in SHRs was eliminated by nephrectomy, but not attenuated by indomethacin, indicating its dependency on renal renin but not on prostaglandin synthesis [38].
• In anesthetized dogs, plasma renin activity and ANG II were measured in arterial and renal venous blood by radioimmunoassay during four periods: control, renal arterial constriction (RAC), angiotensin converting enzyme (ACE) inhibition (MK 422), and MK 422 plus systemic arterial ANG II infusion [39].
• Second, the HR power spectrum was measured in 11 awake rabbits before and after treatment with deoxycorticosterone acetate (1 mg.kg-1.day-1) and salt (0.9% saline ad libitum) for 7 days to depress plasma renin levels [40].

References