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)

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

1. The effects of intrathecal (i.t.) pretreatment with selective B1 or B2 kinin receptor antagonists were studied on the cardiovascular response to i.t. injection of bradykinin (BK) in conscious freely moving rats. 2. BK (81 pmol) produced an increase in mean arterial pressure (MAP: 9-13 mmHg) and decrease in heart rate (HR: 20-30 beats min-1) that reached a maximum 2 min after injection. 3. The BK-induced cardiovascular responses were dose-dependently and reversibly reduced by four antagonists with the following rank order of potency: Tyr, D-Arg[Hyp3,D-Phe7,Leu8]-BK = D-Arg[Tyr3,D-Phe7,Leu8]-BK = D- Arg[Hyp3,D-Phe7,Leu8]-BK > D-Arg[Hyp3,Thi5,D-Tic7,Oic8]-BK (Hoe 140). These compounds failed to alter the cardiovascular response to i.t. injection of 8.1 nmol of substance P. 4. Other compounds acting on the B2 receptor, namely D-Arg[Hyp3,Gly6,Leu8]-BK, D-Arg[Hyp3,D-Phe7]-BK, D-Arg[Hyp2,Thi5,8,D-Phe7]-BK and D-Arg[Hyp3,Gly6,D-Phe7,Leu8]-BK or on the B1 receptor, [Leu8]-desArg9-BK, did not influence the cardiovascular responses to BK at doses devoid of intrinsic activity on MAP and HR. 5. None of the kinin receptor antagonists caused motor impairment, respiratory arrest or persisting cardiovascular changes. 6. These results confirm that the cardiovascular effects induced by i.t. BK are mediated by the activation of a B2 receptor in the rat spinal cord. However, the rank order of potency of antagonists does not conform to the classical B2 functional site characterized in peripheral tissues.
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PMID:Cardiovascular effects of intrathecally administered bradykinin in the rat: characterization of receptors with antagonists. 750 24

NO synthase is present in magnocellular neurons of supraoptic and paraventricular nuclei as well as in the posterior pituitary gland and may participate in control of vasopressin secretion. To test this possibility, experiments were performed in conscious, chronically prepared rabbits to determine the effect of NO synthesis inhibition with NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) on basal vasopressin secretion and vasopressin responses to increased plasma osmolality (hypertonic saline infusion; P osm) and decreased blood pressure (nitroprusside infusion). L-NAME infusion (0.5 mg.kg-1 x min-1 i.v.) increased mean arterial pressure [MAP; 82.6 +/- 3.4 to 93.0 +/- 3.0 mmHg (P < 0.02)], decreased heart rate [HR; 242 +/- 12 to 209 +/- 9 beats/min (P < 0.02)], decreased plasma renin activity [PRA; 3.1 +/- 0.6 to 2.0 +/- 0.6 ng.ml-.2 h-1 (P < 0.001)], and increased plasma vasopressin concentration [P AVP; 2.2 +/- 0.3 to 4.5 +/- 1.0 pg/ml (P < 0.05)]. P(osm) did not change. Hypertonic saline infusion did not change MAP or HR but decreased PRA [4.3 +/- 0.8 to 0.9 +/- 0.2 ng.ml-1 x 2 h-1 (P < 0.01)], increased P(osm) [284 +/- 1 to 305 +/- 2 mosmol/kg H2O (P < 0.001)], and increased PAVP [2.8 +/- 0.3 to 12.7 +/- 2.7 pg/ml (P < 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of inhibition of nitric oxide synthesis on vasopressin secretion in conscious rabbits. 751 50

Since dietary salt loading enhances nitric oxide (NO) generation in the kidney, we investigated the hypothesis that changes in salt intake have specific effects on vascular resistance in the kidney mediated by the L-arginine-NO pathway. We contrasted changes in renal and hindquarter vascular resistances (RVR and HQVR) in anesthetized rats during intravenous infusions of graded doses of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Groups (N = 8 to 10) of rats were maintained on a high salt (HS) or low salt (LS) diet for two weeks. Compared to those on LS, rats on HS had a greater increase in mean arterial pressure (delta MAP; +32 +/- 4 vs. +22 +/- 3%; P = 0.05) and RVR (+160 +/- 17 vs. +83 +/- 10%; P < 0.005) and a greater fall in renal blood flow (delta RBF; -47 +/- 3 vs. -32 +/- 4%; P < 0.01); changes in HQVR were similar in the two groups. The enhanced RVR response to L-NAME in HS rats could not be ascribed to the higher renal perfusion pressure (RPP) since it persisted in rats whose RPP was controlled by adjustment of a suprarenal aortic clamp. Changes in RVR with an NO donor (SIN-1) were similar in HS and LS rats. L-NAME reduced plasma renin activity in both HS and LS rats. After inhibition of ACE with captopril, or of angiotensin II type I (AT1) receptor with losartan, the increase in RVR with L-NAME remained greater in HS than LS rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal vasoconstriction during inhibition of NO synthase: effects of dietary salt. 752 72

In order to find out whether the pressor effect of arginine vasopressin (AVP) is limited by release of nitric oxide (NO) and whether it is altered in hypertension, blood pressure (MAP) and heart rate (HR) responses to i.v. administration of AVP were compared in conscious normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats under control conditions and during blockade of NO synthesis induced by i.v. administration of NG-nitro-L-arginine (L-NOARG). In control experiments AVP elicited significant elevations of MAP in WKY and SHR. The maximum increases in WKY and SHR amounted 26 +/- 3 and 16 +/- 3 mmHg, respectively, and did not differ significantly from each other. In WKY increase of MAP was associated with significant bradycardia. Administration of AVP in this strain during blockade of NO synthesis resulted in significantly smaller increase of blood pressure (13 +/- 5 mmHg) than under control conditions (p < 0.001), and in nonsignificant changes of HR. In SHR AVP caused a progressive significant decrease of blood pressure associated with transient tachycardia. The results indicate that blockade of NO synthesis does not enhance but reduces increase of blood pressure in WKY and transforms the pressor action of this peptide into the hypotensive effect in SHR. This phenomenon is discussed in relevance to the possible unfavorable effects of AVP on coronary and/or cerebral circulation during blockade of NO formation.
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PMID:Effect of NG-nitro-L-arginine on pressor action of arginine vasopressin in normotensive (WKY) and spontaneously hypertensive (SHR) rats. 794 33

The erythropoietin receptor (EpoR) belongs to the cytokine receptor family, members of which lack a tyrosine kinase domain. Recent studies, however, have shown that a cytoplasmic tyrosine kinase, JAK2, interacts with the cytoplasmic domain of the EpoR and becomes activated upon binding of Epo to the receptor. Epo has also been shown to stimulate activation of Ras and Raf-1. The present studies were undertaken to examine the possible involvement of Epo-induced tyrosine phosphorylation in activation of the Ras/mitogen-activated protein kinase (MAP kinase) pathway and to determine its significance on the growth signaling from the EpoR. In an interleukin (IL)-3-dependent cell line expressing the transfected wild-type EpoR, Epo, or IL-3 induced tyrosine phosphorylation of Shc and its association with Grb2. These cytokines also induced tyrosine phosphorylation and activation of MAP kinase isoforms ERK1 and ERK2. A mutant EpoR with a carboxyl-terminal deletion of 108 amino acids (H mutant), which is mitogenically functional but lacks tyrosine phosphorylation sites in the carboxyl-terminal region, showed markedly diminished abilities to induce tyrosine phosphorylation of Shc and to phosphorylate and activate MAP kinases. A mutant receptor (PM4 mutant) inactivated by a point mutation, Trp282 to Arg, which abrogates the interaction with JAK2, failed to induce any effect on Shc or MAP kinases. In cells expressing a mutant EpoR that is constitutively activated by a point mutation, Arg129 to Cys, in the extracellular portion of the receptor, neither tyrosine phosphorylation of Shc nor activation of MAP kinases by phosphorylation was detectable without stimulation with Epo or IL-3. These results suggest that the carboxyl-terminal region of EpoR may play a crucial role in activation of MAP kinases through the Ras signaling pathway which may be activated by tyrosine phosphorylation of Shc and its association with Grb2. The activation of MAP kinases, however, failed to correlate with the mitogenic activity of mutant EpoRs and thus may not be required for growth signaling from the EpoR.
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PMID:Activation of the mitogen-activated protein kinase pathway by the erythropoietin receptor. 796 95

To compare the contribution of nitric oxide (NO) to the buffering of short-term and circadian fluctuations of arterial blood pressure with that of the baroreceptor reflex, conscious foxhounds were subjected to continuous 24-h blood pressure recordings. A pressure transducer was placed into the lumen of the abdominal aorta. Telemetry recordings were done under control conditions, following blockade of NO formation by intravenous bolus injection of NG-nitro-L-arginine (L-NNA; 16.5 +/- 2 mg/kg body wt) and after total sinoaortic and cardiopulmonary denervation in five dogs each. L-NNA produced a sustained elevation of mean arterial pressure (MAP; 137.2 +/- 6.4 mmHg vs. control, 112.9 +/- 3.7 mmHg). After denervation, no significant increase of MAP was found (113.5 +/- 4.1 mmHg), but the standard deviation of the MAP histogram was significantly greater (22.5 +/- 3.1 vs. 10.6 +/- 0.9 mmHg, P < 0.05). Sequential spectral analysis showed that total power between 0 and 0.5 Hz was elevated more than twofold after L-NNA (P < 0.05). This was due primarily to increased power in the range above 0.1 Hz. After denervation, total power increased about three-fold (P < 0.05), almost exclusively occurring below 0.04 Hz. Power in the range above 0.2 Hz was diminished, although not significantly. It is concluded that in the conscious dog, NO, as well as the baroreceptor reflex, is an effective blood pressure buffer. NO is most effective above 0.1 Hz, whereas the baroreceptors primarily buffer fluctuations slower than 0.04 Hz.
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PMID:The blood pressure buffering capacity of nitric oxide by comparison to the baroreceptor reflex. 806 5

In up to 60% of women with chronic renal disease an elevation of blood pressure is seen during pregnancy. The pathogenesis of this complication may be related to a diminished synthesis of vasodilatory substances by endothelial cells and to an increased sensitivity to vasopressor hormones such as angiotensin II. Previous experimental studies in rats with early chronic renal disease (adriamycin nephropathy, AN) have shown that this pregnancy-induced hypertension is associated with a lowered synthesis of glomerular PGE2. In the present study the vascular response to vasoactive substances was evaluated. In AN rats the sensitivity to an acute infusion of angiotensin II was augmented, whilst it was blunted in normal pregnant rats. Chronic treatment with the thromboxane-(Tx)-receptor antagonist, daltroban (60 mg/kg/day, p.o.) administered from mid-pregnancy induced a similar reduction in blood pressure in both AN virgin and pregnant rats. This suggests that adriamycin per se may induce vascular damage which may interfere with the normal vascular adaptation to pregnancy. Stimulation of NO synthesis with L-arginine decreased MAP values significantly in PAN rats but did not modify them during normal pregnancy. In additional experimental inhibition of the endothelial-derived relaxing factor (EDRF), nitric oxide (NO) synthesis with NAME from mid-pregnancy significantly increased SBP and MAP in normal rats. By contrast, in PAN rats chronic NAME treatment had no effect. In summary, the development of hypertension in pregnant rats with AN may be associated to endothelial cell dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pregnancy-induced hypertension in rats with early adriamycin nephropathy. 807 19

The hemodynamic actions of N-nitro-L-arginine (L-NNA), a novel NO synthesis inhibitor, and its effect on renal sympathetic nerve activity (RSNA) were examined in anesthetized rats to define the possible role of L-NNA in the regulation of blood pressure and the underlying mechanism(s). The results obtained were as follows. (1) Following intravenous bolus injection of L-NNA (15 mg/kg), MAP was changed from 9.87 +/- 0.80 to 14.67 +/- 0.53 kPa (P < 0.001), HR from 317 +/- 13 to 303 +/- 14 bpm, CI from 9.79 +/- 0.83 to 7.04 +/- 0.41 ml/min.100 g-1 (P < 0.05), and TPRI from 1.04 +/- 0.10 to 2.15 +/- 0.18 u/100 g (P < 0.001), all lasting for more than 30 min. The above-mentioned actions of L-NNA could be inhibited by prior administration of L-arginine (200 mg/kg). (2) In rats with sinoaortic denervation (SAD), i.v. L-NNA might induce an increase in HR, indicating that L-NNA-induced bradycardia was resulted from a baroreceptive activation. (3) In rats with buffer nerves intact, i.v. L-NNA failed to induce a significant change in RSNA, though an increase in MAP accompanied by bradycardia was observed. (4) With i.v. L-NNA for SAD rats, MAP, HR and RSNA were markedly increased by 55.6%, 5.1% and 34.3%, respectively. The results implied that L-NNA was able to activate sympathetic center, and L-NNA-induced change of RSNA could be masked by baroreflex. Prior administration of L-arg was capable of inhibiting the effect of L-NNA on RSNA in SAD rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamic actions of N-nitro-L-arginine and its effect on renal sympathetic nerve activity in anesthetized rats]. 814 66

Competitive inhibition of the conversion of L-arginine to nitric oxide by a high dose of NG-monomethyl-L-arginine (L-NMMA) leads to significant increases in arterial pressure, natriuresis, and diuresis in Sprague-Dawley rats. The purpose of this study was to determine the extent of the natriuretic and diuretic responses and the possible role of arterial pressure and renal interstitial hydrostatic pressure (RIHP) elevations with the infusion of L-NMMA in anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Intravenous infusion of L-NMMA (15 mg/kg bolus followed by 500 micrograms.kg-1.min-1 continuous infusion) in WKY rats (n = 8) resulted in a significant increase in mean arterial pressure (MAP, 122 +/- 3 to 152 +/- 2 mmHg), RIHP (4.7 +/- 0.4 to 6.7 +/- 0.5 mmHg), fractional excretion of sodium (FENa, 0.76 +/- 0.21 to 4.74 +/- 0.70%), and urine flow rate (V, 27.7 +/- 5.0 to 161.3 +/- 19.6 microliters/min). Increases in RIHP and sodium and water excretions are abolished when renal perfusion pressure is prevented from increasing with L-NMMA infusion in a group of WKY rats (n = 6). In SHR (n = 6) administration of the same dose of L-NMMA resulted in no significant changes in MAP (172 +/- 3 to 178 +/- 2 mmHg) or RIHP (3.3 +/- 0.4 to 3.5 +/- 0.6 mmHg), but significantly higher increases in FENa (1.19 +/- 0.26 to 7.52 +/- 0.68%) and V (47.1 +/- 10.0 to 248.3 +/- 25.7 microliters/min) compared with WKY rat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of nitric oxide causes exaggerated natriuresis in spontaneously hypertensive rats. 820 60


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