Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in situ heart is exposed to blood-borne vasoconstrictor agents (e.g., vasopressin) which, if unopposed, may cause radically increased coronary vascular resistance (CVR). Release of endogenous vasodilator, such as prostacyclin (PGI2), is a possible mitigating mechanism. We investigated the ability of the heart to maintain CVR within a narrow range when exposed to exogenous vasoconstrictors. The isolated rat heart was perfused at constant flow rate (5-6 ml/min) with oxygenated Krebs-Ringer bicarbonate solution (37 degrees C, pH 7.4), and was rendered quiescent by a local injection of lidocaine to the atrio-ventricular node. Changes of perfusion pressure, indicating changes of CVR, were monitored and the cardiac effluent was collected for analysis of 6-keto PGF1 alpha and thromboxane B2 (stable metabolites of PGI2 and thromboxane A2, respectively) by radioimmunoassay. Hearts were infused with four different vasoconstrictors (i.e., serotonin, vasopressin, angiotensin II and the thromboxane A2/PGH2 mimetic, U46619). There was a linear relationship between the dose-dependent increase in CVR and PGI2 production in serotonin, U46619 and vasopressin-infused quiescent heart. Vasoconstriction induced by angiotensin II was not dose-dependent and was unrelated to PGI2 production. Thus, PGI2 is produced in response to coronary vessel constriction, presumably to mitigate the constriction. No detectable thromboxane B2 was released by any of these vasoconstrictors. Partial inhibition (approximately 50%) of PGI2 production by aspirin (5.6 microM) treatment resulted in a paradoxically decreased vasoconstriction except at the lowest level of serotonin and vasopressin. Aspirin (1 mM) greatly reduced PGI2 production (approximately 90%) but the fall in CVR persisted.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of exogenous vasoconstrictors on coronary vascular resistance and prostacyclin production of the quiescent heart: the inhibitory effect of aspirin. 249 43

The effects of the recently described human alpha-calcitonin gene-related peptide (CGRP), human beta-CGRP and rat alpha-CGRP have been compared with those of the vasodilator sodium nitroprusside, on the rat and rabbit isolated heart. Hearts were perfused at constant flow and [Arg8]-vasopressin was used to increase coronary perfusion pressure. In the rat heart, the order of potency for evoking cumulative dose-dependent falls in perfusion pressure was human beta-CGRP greater than rat alpha-CGRP greater than human alpha-CGRP greater than sodium nitroprusside. In the same preparations the three CGRPs (but not sodium nitroprusside) elicited cumulative dose-related increases in heart rate. In the rabbit heart the order of potency for vasodilatation was rat alpha-CGRP greater than human alpha-CGRP greater than sodium nitroprusside. In marked contrast to results from the rat, neither rat alpha-CGRP nor human alpha-CGRP altered heart rate in the rabbit isolated heart. These results show that human alpha- and beta-CGRP and rat alpha-CGRP are vasodilators in the coronary vasculature, but that there is species variation as CGRP had a positive chronotropic effect in the rat heart but not in the rabbit heart.
 ...
PMID:Human alpha- and beta-CGRP and rat alpha-CGRP are coronary vasodilators in the rat. 348 43

The present study investigated how variations in coronary vascular resistance and metabolic demand affected myocardial capillary diffusion capacity. Hearts from Wistar rats were perfused with Krebs-Henseleit-albumin buffer in a Langendorff preparation, where heart rate (HR), contractility (dP/dtmax) and myocardial oxygen consumption (MVO2) were recorded continuously. Myocardial capillary diffusion capacity was measured as the permeability surface area product (PS) for Cr-EDTA and vitamin B12 by the single injection colorimetric indicator dilution method. After base-line recordings without drugs, angiotensin II+Arginine-vasopressin was infused, which increased coronary vascular resistance by 90%, stimulated HR by 11%, decreased dP/dtmax by 21% and reduced MVO2 by 4%. PSCr-EDTA and PSB12 decreased by 24 and 27%, respectively, leaving the ratio PSCr-EDTA/PSB12 unchanged indicating unaltered capillary permeability. Moreover, the reductions in MVO2 and PS correlated significantly. During vasodilation: (1) nitroprusside-NA stimulated HR by 7% and decreased dP/dtmax by 14%; (2) adenosine reduced dP/dtmax by 37% and decreased MVO2 by 9%; and (3) isoproterenol increased HR, dP/dtmax and MVO2 by 53, 76 and 9%, respectively. However, all three vasodilators reduced PSCr-EDTA and PSB12 in parallel by 7-25% leaving PSCR-EDTA/PSB12 unchanged. Thus, maximal estimated diffusion capacities were obtained during spontaneous coronary vascular tone, most likely reflecting maximal capillary recruitment in the Krebs-Henseleit-albumin perfused heart. The derecruiting effects of the vasoconstrictors were partly overridden by metabolic factors, while the reductions of PS after vasodilation more likely were due to increased heterogeneity in coronary flow.
 ...
PMID:Changes in myocardial capillary diffusion capacity during infusion of vasoactive drugs. 845 41

Male Wistar rats received intraperitoneal injections of physiological saline (control), phenamine, fentanyl, ethanol, sodium ethaminal, or dexamethasone in increasing concentrations for 4 days. Forced administration of these drugs provided gradual load of the organism and prevented the development of tolerance. Such approach is extensively used for the development of drug addiction or several manifestations of this state. Expression of corticotropin-releasing hormone mRNA in the amygdala was maximum after administration of dexamethasone (0.46 arb. units vs. beta-actin), but was much lower in experiments with sodium ethaminal and fentanyl (0.07 and 0.037 arb. units, respectively). In the hypothalamus, enhanced mRNA expression was observed after injection of sodium ethaminal, ethanol, and fentanyl (0.8, 0.37, and 0.039 arb. units, respectively). Phenamine did not increase mRNA expression in the amygdala and hypothalamus. Expression of vasopressin mRNA was not detectable in brain structures of animals from various groups. Our results indicate that the hypothalamic reinforcement system provides a similar response to narcogens, whereas the extended amygdala includes elements of both reinforcement and stress reactivity.
 ...
PMID:Expression of mRNA for corticotropin-releasing hormone and vasopressin in the hypothalamus and amygdala of rats after administration of narcogenic. 1924 Aug 49