Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 12 patients with essential hypertension who remained hypertensive despite chronic chlorthalidone treatment, the effect of 2 weeks of additional therapy with the converting enzyme inhibitor (CEI) enalapril on blood pressure and body fluid volumes has been evaluated. The objective was to examine the influence of a diuretic-stimulated renin-angiotensin-aldosterone system (RAAS) on haemodynamics and body fluid volume. Mean arterial pressure (MAP -21%), total peripheral resistance index (TPRI -22%) and plasma aldosterone concentration (PAC -39%) were decreased, and plasma renin activity (PRA 660%) was increased. The average heart rate (HR), cardiac index (CI), plasma volume (PV), blood volume (BV), extracellular fluid volume (ECFV) and body weight (BW) remained unchanged. A negative correlation was found between the per cent changes in ECFV and PAC. Thus, body fluid volumes during chronic diuretic treatment are well preserved even when the RAAS with its sodium retaining properties is suppressed by CEI. Possible mechanisms are a volume (not angiotensin II) - dependent stimulation of aldosterone and a fall in blood pressure.
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PMID:Changes in haemodynamics and body fluid volume due to enalapril in patients with essential hypertension on chronic diuretic therapy. 302 15

Chronically catheterized fetal lambs (n = 11, gestational age 111-139 days) and neonatal lambs (n = 20, postnatal age 4-30 days) were studied to explore during development the relationship of renal hemodynamic responses during hypoxemia to plasma epinephrine concentration (E), plasma norepinephrine concentration (NE), plasma arginine vasopressin concentration (AVP), and plasma renin activity (PRA). A low oxygen gas mixture (11.1 +/- 0.1% O2) was administered for 30 min to the pregnant ewe or neonatal lamb to induce hypoxemia with maintenance of normal arterial pCO2 and pH. Arterial blood pressure was recorded continuously and renal blood flow (RBF) was determined by the radiolabeled microsphere technique. Moderate hypoxemia (pO2 16 +/- 2 torr and 33 +/- 6 torr in fetus and neonate, respectively) induced increases in E, NE (measured by radioenzymatic assay), and AVP (measured by radioimmunoassay) in both fetus and neonate. PRA (measured by radioimmunoassay) also increased in response to hypoxemia in neonatal lambs. The change in mean arterial pressure with hypoxemia (delta MAP) was significant in fetuses (delta MAP 8 +/- 14%, p less than 0.05) but not in lambs (delta MAP 1 +/- 10%, p greater than 0.5). Similarly, the change in renal blood flow with hypoxemia (delta RBF) was significant (delta RBF -51 +/- 24%, p less than 0.001) in fetuses but not in neonatal lambs (delta RBF -9 +/- 38%, p greater than 0.1). These results reflected a change in renal vascular resistance with hypoxemia (delta RVR) that was significant in fetal lambs (delta RVR 169 +/- 168%, p less than 0.01) but not in neonatal lambs (delta RVR 51 +/- 180%, p greater than 0.2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal hemodynamic responses to hypoxemia during development: relationships to circulating vasoactive substances. 328 Nov 20

The isolated and combined influence of cardiopulmonary and sinoaortic denervation on long-term blood pressure (MAP), heart rate (HR), plasma renin activity (PRA) and plasma volume (PV) was studied in 11 conscious, chronically instrumented foxhounds receiving a normal sodium diet. MAP, HR, PV and PRA remained unchanged in the 5 dogs after bilateral thoracic vagal stripping, which eliminates the cardiopulmonary afferents. After sino-aortic denervation in another 5 dogs there was equally little change when compared to the control group. Only total baroreceptor and cardiopulmonary denervation (7 dogs) revealed significantly higher levels of MAP (119.6 +/- 4.6 vs. 100.4 +/- 1.5, P less than 0.01), HR (118.2 +/- 3.7; vs. 84.1 +/- 3.5; P less than 0.0001), and PRA (3.6 +/- 0.9 vs. 0.9 +/- 0.2; P less than 0.05). In conclusion, the function of either arterial baroreceptors or cardiopulmonary receptors is sufficient for normal circulatory control. When both groups of receptor afferents are interrupted, MAP, HR, and PRA rise to significantly higher levels. Thus, both systems interact in a sense of a non-additive attenuation on "cardiovascular centres". This may clarify previous disputes concerning neurogenic hypertension, and supplies information for the role of the renin-angiotensin system in blood pressure control.
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PMID:Effect of sino-aortic denervation in comparison to cardiopulmonary deafferentiation on long-term blood pressure in conscious dogs. 328 22

The isolated and combined influence of cardiopulmonary and arterial baroreceptor denervation on long-term blood pressure (MAP), heart rate (HR), plasma volume (PV) and plasma renin activity (PRA) was studied in 10 conscious, chronically instrumented foxhounds receiving a normal sodium diet. Cardiopulmonary denervation was achieved by surgically stripping both thoracic vagi. Near complete arterial baroreceptor denervation, leaving most cardiopulmonary fibres intact, was made by left vagal deafferentiation which has been shown to eliminate most aortic baroreceptor afferents, and a carotid sinus denervation. Five groups were studied: (I) control (n = 9), (II) cardiopulmonary denervation (n = 5), (III) aortic baroreceptor denervation (n = 5), (IV) arterial baroreceptor denervation (n = 4) and (V) total denervation (n = 6). No changes in PV were observed. Only group V revealed significantly higher levels of MAP (119.5 +/- 5.4 vs. 100.1 +/- 1.6 mmHg; P less than 0.05), HR (118.1 +/- 4.4 vs. 87.8 +/- 3.7 beats min-1; P less than 0.001) and PRA (3.0 +/- 0.8 vs. 0.9 +/- 0.2 ng AI m-1 h-1; P less than 0.05). It is suggested that the isolated function of either cardiopulmonary or arterial baroreceptors is sufficient to maintain these variables at a normal level. Contrary to the results of other reports the cardiopulmonary receptors do not seem to regulate MAP at a level about which the arterial baroreceptors operate. When both groups of afferents were interrupted MAP, HR and PRA rose to significantly higher levels, implying that cardiopulmonary and arterial baroreceptor afferents interact in a sense of a non-additive attenuation.
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PMID:The influence of cardiopulmonary receptors on long-term blood pressure control and plasma renin activity in conscious dogs. 330 4

In 12 conscious dogs on a normal sodium diet the renal venous-arterial plasma renin activity-difference as a function of mean renal artery pressure (renin stimulus-response curve; RSRC) as well as long-term mean arterial blood pressure (MAP; pressure-histograms) were measured repeatedly. The RSRC has 1) a threshold pressure (Pth), 2) a flat section above Pth (plateau-level), and 3) a steep slope below Pth. From dog to dog the slope varied from -0.20 to -0.54 ng AI/ml/h/mmHg and Pth from 78.4 to 107.1 mmHg. In every dog MAP was higher than Pth (MAP-Pth:12.8 +/- 1.58 mmHg). Dogs with a higher Pth regularly showed a higher MAP (r = 0.76; P less than 0.005). Due to its normal variability arterial pressure occasionally falls below Pth and thus causes renin release. Therefore MAP will stabilize at a level above Pth. The pressor effect (MAP-Pth) of this feedback system should depend on the sensitivity of the pressure-dependent renin release mechanism (slope of RSRC). Accordingly we observed a close correlation between the slope of the RSRC and the MAP-Pth difference (r = 0.93; P less than 0.0001). We conclude that in healthy dogs the level of long-term blood pressure can be explained almost completely by Pth and the slope of the pressure-dependent renin release. Our findings may offer new perspectives to the pathogenesis of hypertension.
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PMID:Pressure-dependent renin release: the kidney factor in long-term control of arterial blood pressure in conscious dogs. 331 25

The rapid fall in blood pressure after removal of the constricting clip in two-kidney one-clip (2K-1C) hypertension in the rat is not fully explained by inhibition of the renin-angiotensin system or change in sodium balance. It has been postulated that compounds released in the renal venous effluent following unclipping of 2K-1C rats have a central opiate-like action and endogenous opioids are recognized to have profound hypotensive properties. To investigate this, we removed the clip from, or performed a sham operation in, early phase (less than 6 weeks) 2K-1C hypertensive rats during an infusion of naloxone, an opioid antagonist, or vehicle alone. The infusion of naloxone did not affect the pattern of blood pressure fall in either unclipped or sham-operated rats. Both naloxone-treated and control groups were similarly normotensive at 24 hr postoperation, the MAP being significantly lower than in the sham-operated groups, which regained previously hypertensive levels. Heart rate was unchanged 24 hr postoperatively in all groups. Morphine-induced bradycardia and hypotension were significantly reduced by naloxone infusion. Thus, naloxone infusion had no effect on blood pressure or heart rate in either the sham-operated or the unclipped groups, indicating that endogenous opioids do not have a major role in the reversal of renovascular hypertension under these circumstances.
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PMID:Failure of naloxone to influence surgical reversal of two-kidney, one-clip hypertension in the rat. 354 Sep 75

Forty-two spontaneously hypertensive rats (SHR) and 42 normotensive Wistar-Kyoto rats (WKY) were anesthetized with either halothane or enflurane. Blood pressure, heart rate, cardiac output, distribution of blood flow, plasma renin activity, and plasma catecholamines were measured to determine in what manner the hypertensive animal responded to these two anesthetics. Major findings of the study were that plasma renin activity did not increase in the SHR despite a 25% reduction in MAP. The infusion of saralasin, an angiotensin II antagonist, resulted in a further decrease in blood pressure in SHR anesthetized with halothane but not with enflurane. Plasma catecholamine concentrations were elevated in the awake SHR and were decreased in SHR anesthetized with enflurane. Both halothane and enflurane anesthesia resulted in similar alterations in blood flow in the SHR. The normotensive WKY responded to halothane and enflurane in a different manner than the SHR. Plasma renin activity increased with the decrease in blood pressure with both agents. A further decrease in blood pressure occurred with saralasin infusion in WKY anesthetized with halothane or enflurane. Significant blood flow alterations occurred in the WKY anesthetized with both agents, but enflurane caused the greatest changes. The SHR may prove useful in examining the effects of anesthetic agents and other drugs so that we may have a better understanding of the perioperative management of the patients with essential hypertension.
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PMID:Hormonal and hemodynamic responses to halothane and enflurane in spontaneously hypertensive rats. 388 21

Sixteen patients (11 M, 5 F), median age 41 years, with essential hypertension insufficiently controlled on hydrochlorothiazide 75 mg/day (DBP greater than or equal to 100 mmHg) were investigated. Plasma renin concentration (PRC), angiotensin II concentration (PA II), aldosterone concentration (PAC), plasma noradrenaline concentration (PNAC), plasma volume (PV) and exchangeable sodium (NaE) were determined and a saralasin-infusion (5.4 nmol/kg/min) was carried out while the patients were on thiazide alone, and in fourteen cases, repeated 3 months later after addition of a beta-blocker (propranolol 6, metoprolol 6 and atenolol 2 patients). On thiazide alone PRC, PA II and PAC was higher than normal in the group as a whole and the angiotensin II-inhibitor, saralasin, caused a significant decrease in MAP in twelve out of sixteen patients. After addition of a beta-blocker SBP and DBP decreased from 164/109 mmHg to 136/94 mmHg. PRC and PA II decreased by 40% and 58%, respectively. At this point saralasin caused no significant change in MAP. No close correlation was found between changes in BP on beta-blocker treatment and either PRC, PA II or saralasin response on thiazide treatment. PV, NaE, PAC and PNAC did not change sigificantly. It is concluded that in pts with thiazide-induced stimulation of the renin-angiotensin system (RAS) addition of a beta-blocker leads to suppression of RAS and the angiotensin II dependence of the blood pressure is nearly abolished. This mechanism might well contribute to the antihypertensive effect of beta-blockade in this particular situation. However, the pharmacological changes induced by beta-blockade are very complex, and most likely other factors are involved in the antihypertensive effect of beta-blocking drugs.
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PMID:Angiotensin II blockade during combined thiazide-beta-blocker treatment. 610 82

The effects of phentolamine, KBIV24 and captopril on the mean arterial blood pressure of normal and treated (dehydration, hemorrhage) frogs were determined. Hemorrhage but not dehydration led to a decrease in MAP. Only phentolamine attentuated MAP in both normal and treated frogs. KBIV24 and captopril were ineffective. It was concluded that the blood pressure of frogs is regulated by catecholamine. Neither arginine vasotocin nor the renin-angiotensin system play any role in blood pressure homeostasis in normal and hypovolemic conditions.
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PMID:Blood pressure homeostasis in Rana catesbeiana under normal and hypovolemic conditions. 615 57

The effect of saralasin infusion on systemic hemodynamics, plasma renin activity (PRA), and aldosterone levels was studied under various conditions of sodium balance in 25 patients with essential hypertension. The results of 66 paired observations were statistically analyzed, to elucidate some controversial aspects of the mechanisms of saralasin action. The total peripheral resistance index (TPRI) increased when saralasin had an agonistic effect on blood pressure (BP) and decreased when it acted as an antagonist. The TPRI changed more than the BP by an inversely directed change in the cardiac index (CI). In addition, the changes in the CI were only weakly correlated with the changes in MAP; CI decreased consistently when BP increased but showed no distinct pattern when saralasin acted as an antagonist. The pulse rate did not change under any of the conditions applied. The present findings suggest that in addition to its antagonistic effects on peripheral circulation, saralasin has some action on the heart and autonomic nervous system. The observed changes in the plasma aldosterone level were in accordance with the changes in TPRI and did not point to a difference between adrenal and vascular sensitivity to saralasin or angiotensin II. The overall hemodynamic responses were related to the existing level of PRA. No correlation was found between the degree of volume depletion and the blood pressure response during saralasin after elimination of the effect of PRA by partial regression analysis. These findings do not support the concept that more information about the renin dependency of the BP is provided by the BP reaction to saralasin than by determination of the PRA.
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PMID:Systemic hemodynamic and hormonal responses during angiotensin II blockade with saralasin. 616 55


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