Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is evidence of an intrinsic renin-angiotensin system in the brain. The goal of the study was to determine whether stimulation of endogenous angiotensin production by applying renin to the brain surface has an effect on pial arteriolar caliber and CBF. Pial vessel diameters were measured through a closed cranial window in anesthetized rabbits. Percent changes of blood flow in the cortical area under the cranial window were simultaneously measured by laser-Doppler flowmetry. Topical application of 0.01-0.1 U/ml renin induced maximum dilation of 18.9 +/- 4% (mean +/- SD) of pial arterioles within 2 min. Arteriolar calibers thereafter decreased slowly. Flow gradually increased to peak at 38 +/- 15% 50 min after renin application. Angiotensin I levels in jugular blood, as measured by radioimmunoassay, increased to a peak 40 min after topical renin application. Angiotensin II levels in jugular blood and both angiotensin I and II levels in blood samples from the femoral artery did not change. Diameter and flow changes were inhibited by intravenous pretreatment with the converting enzyme blocker captopril (10 mg/kg body wt i.v.). Captopril did not affect the vasodilation and flow increase in response to hypercapnia. Topically applied captopril (10(-5) M) blocked renin-induced arteriolar dilation. We conclude that renin increases pial arteriolar diameters and cortical blood flow in the rabbit brain. Stimulation of angiotensin production is likely to be a mediator of this response.
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PMID:Effect of renin on brain arterioles and cerebral blood flow in rabbits. 896 12

1. It has been proposed that hypertension alters the respiratory and cardiovascular responses to chemoreceptor stimulation. However, in studies of human hypertension or in genetic animal models of hypertension it has been difficult to unequivocally attribute the changes to hypertension per se, rather than to a genetic predisposition towards an altered chemoreflex response independent of hypertension. 2. In the present study a group of seven rabbits were made hypertensive via a continuous 7 week infusion of angiotensin II (AngII; 50 ng/kg per min, i.v.). Animals were studied twice before AngII treatment commenced, twice during infusion and 48 h after stopping infusion. At each of these times the relationship between heart rate (HR) and mean arterial pressure (MAP) was determined under normoxic, acute hypoxic (10% O2 + 3% CO2) and acute hypercapnic (18% O2 +, 6.5% CO2) conditions for 20 min. A group of six animals also served as time controls. 3. Angiotensin II infusion increased arterial pressure from control levels of 80 +/- 2 to 114 +/- 8 mmHg and maintained it at this level throughout the 7 week period. After 1 week of AngII infusion there was a rightward shift in the heart rate-baroreflex curve, indicating that the baroreflex was now operating at an increased level of pressure. These changes were associated with reductions in the gain from -7.6 +/- 1.6 to -3.0 +/- 0.2 b.p.m./ mmHg, HR range and curvature of the baroreflex. These effects were maintained throughout the 7 weeks of hypertension and were reversed within 2 days of ceasing AngII infusion. Acute hypoxia and hypercapnia in normotensive animals caused a reduction in the HR range of 19 +/- 7 and 15 +/- 7 b.p.m., respectively, but caused no change in the gain (sensitivity) of the baroreflex. Despite the marked changes in the baroreflex produced by the hypertension, the effect of hypoxia or hypercapnia on the HR baroreflex was not different in the hypertensive group. 4. It is concluded that chronic experimental AngII-based hypertension does not alter the HR baroreflex response to hypoxia or hypercapnia and suggests that the altered responses seen in other studies is due to a genetic predisposition as opposed to the effect of raised arterial pressure.
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PMID:Baroreflex control of heart rate during hypoxia and hypercapnia in chronically hypertensive rabbits. 913 Dec 90

1. The placental vascular bed is normally fully dilated. Therefore, changes in vascular resistance elsewhere in the body can affect uteroplacental blood flow (UBF). For example, antihypertensive drugs, such as diazoxide, hydralazine and the angiotensin-converting enzyme inhibitor captopril, cause falls in arterial pressure and, hence, in UBF. 2. Angiotensin II (AngII), prostacyclin and nitric oxide (NO) all influence uteroplacental vascular tone. Angiotensin II in a pharmacological dose (62.5 micrograms/h) had a biphasic effect on UBF in the sheep. Initially, there was a rise in UBF as pressure rose; however, by 16-24 h, UBF had fallen. The AngII-induced fall in UBF caused severe foetal hypoxia and hypercapnia. 3. Prostacyclin may protect the uteroplacental circulation from vasoconstrictors such as AngII, as the vasoconstrictor effect of AngII in the uteroplacental circulation is enhanced following indomethacin. 4. Oestrogen-induced uterine artery vasodilation is nitrergic dependent. As well, nitrergic nerves alter the responsiveness of pregnant uterine arteries to noradrenaline. 5. Thus, both systemic and local factors are important in the control of UBF and in promoting foetal health and growth.
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PMID:Effects of drugs on uteroplacental blood flow and the health of the foetus. 936 71

Angiotensin II (AngII) is an important vasoconstrictor during hypovolemia. This study focused on the effects of the AngII receptor blocker candesartan on intestinal, hepatic, and renal hemodynamics during severe hypovolemia when administered in preexisting moderate hypovolemia. It was hypothesized that specific AngII receptor blockade might enhance splanchnic perfusion during hypovolemia. Fasted, anesthetized, ventilated, juvenile pigs were hemorrhaged by 20% of the blood volume for 30 min. Animals were then randomized to receive candesartan (CAND, n = 11) or the vehicle (CTRL, n = 10) prior to further hemorrhage to 40% of the blood volume for 30 min. The shed blood was then retransfused. Systemic and splanchnic hemodynamics were recorded including intestinal mucosal, superficial and parenchymal hepatic, and cortical and medullary renal microcirculation by laser-Doppler flowmetry. Arterial blood gases were analysed. Candesartan-treated animals maintained mesenteric and jejunal mucosal perfusion during 40% hypovolemia compared to CTRL animals, while no differences were observed in the hepatic and renal circulation. Retransfusion restored mesenteric and renal blood flows despite persistent hypotension and reduced cardiac output in both CAND and CTRL animals. Renal medullary and hepatic parenchymal microcirculation failed to recover during retransfusion in both CAND and CTRL animals. Arterial acidosis, hypercarbia, and a negative base excess were observed in CTRL animals following retransfusion whereas those parameters were normalised in CAND animals. Administration of candesartan in moderate hypovolemia ameliorated the reduction and consequences of mesenteric and intestinal, but not hepatic perfusion during severe hypovolemia. No adverse effects were observed in the renal circulation.
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PMID:Angiotensin II blockade in existing hypovolemia: effects of candesartan in the porcine splanchnic and renal circulation. 1104 12