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At least 127 records · Page 7Linked to original sources
PubMed1996

Central nicotinic receptor blockade inhibits emotionally conditioned pressor responses in rats.

A conditioned stimulus previously paired with electric footshock produced an increase in blood pressure in conscious, freely moving rats. The conditioned pressor response was reproducible. Intracerebroventricular injection of the nicotinic receptor antagonists hexamethonium (1-10 micrograms) or pentolinium (10 micrograms) but not the muscarinic receptor antagonist methylatropine (3 micrograms) produced an inhibition of the conditioned pressor response, whereas intraarterial injection of hexamethonium (10 micrograms) did not affect the response. Intraventricular injection of the cholinesterase inhibitor physostigmine (3-10 micrograms) produced an enhancement of the conditioned pressor response. These results are consistent with the possibility that central nicotinic receptors play a role in the expression of the emotionally conditioned pressor response in rats.

Animals↗
PubMed1976

Effect of acetylcholine on melanophores of Rana tigrina.

Acetylcholine produced melanin aggregation and blanching of skin colour in Rana tigrina, the common Indian frog. The effects were more prolonged in frogs pretreated with an anticholinesterase agent. Acetylcholine effects were not antagonized by either m-cholinolytic (atropine) or n-cholinolytic (pentolinium) agents, but were markedly inhibited by procaine. The results have been discussed in the light of the well-known membrane-stabilizing effect of procaine.

Acetylcholine↗
PubMed2002

Resolving the composite trait of hypertension into its pharmacogenetic determinants by acute pharmacological modulation of blood pressure regulatory systems.

Acute pharmacogenetic analysis was carried out in an intercross F2 population derived from Prague hypertensive-hypertriglyceridemic and Lewis rats. Quantitative trait loci (QTL) mapping was performed for baseline blood pressure (BP) and for BP after blockade of the renin-angiotensin system by losartan, of the sympathetic nervous system (SNS) by pentolinium, and of the nitric oxide system by N(G)-nitro- L-arginine methyl ester. Two significant loci for baseline BP were found on chromosome (Chr) 3 (logarithm of likelihood, LOD, 3.8) and Chr 5 (LOD 3.6), and one suggestive locus on Chr 1 (LOD 2.7). The QTL on Chr 3 persisted after treatment with the three agents while the QTL on Chr 5 and Chr 1 disappeared after pentolinium administration. This suggests independence of the locus on Chr 3 from each acute BP regulatory system examined, whereas the loci on Chr 5 and Chr 1 appeared to be controlled mainly by the SNS. Although not apparent at baseline, a significant locus appeared on Chr 8 (LOD 7.0) after blockade of the SNS, and NO system blockade led to the appearance of a new QTL on Chr 1 (LOD 3.6), indicating the contribution of the inhibited systems to these loci. Pharmacogenetic dissection of the BP trait is a powerful tool to unravel the underlying physiological mechanisms of QTL affecting baseline BP and to identify specific QTL for the response to drugs. This pharmocogenetic approach enabled us to determine the main causative acute BP regulatory systems and should lead to better selection of suitable antihypertensive drugs for individual patients.

Animals↗
PubMed2006

The participation of brain NO synthase in blood pressure control of adult spontaneously hypertensive rats.

Increased blood pressure (BP) in genetic hypertension is usually caused by high activity of sympathetic nervous system (SNS) which is enhanced by central angiotensin II but lowered by central nitric oxide (NO). We have therefore evaluated NO synthase (NOS) activity as well as neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS) protein expression in brainstem and midbrain of adult spontaneously hypertensive rats (SHR) characterized by enhanced sympathetic vasoconstriction. We also studied possible participation of brain NO in antihypertensive effects of chronic captopril treatment of adult SHR. NOS activity was increased in midbrain of SHR compared to Wistar-Kyoto (WKY) rats. This could be ascribed to enhanced iNOS expression, whereas nNOS expression was unchanged and eNOS expression was reduced in this brain region. In contrast, no significant changes of NOS activity were found in brainstem of SHR in which nNOS and iNOS expression was unchanged, but eNOS expression was increased. Chronic captopril administration lowered BP of adult SHR mainly by attenuation of sympathetic tone, whereas the reduction of angiotensin II-dependent vasoconstriction and the decrease of residual BP (amelioration of structural remodeling of resistance vessels) were less important. This treatment did not affect significantly either NOS activity or expression of any NOS isoform in the two brain regions. Our data do not support the hypothesis that altered brain NO formation contributes to sympathetic hyperactivity and high BP of adult SHR with established hypertension.

Animals↗
PubMed1985

Brainstem activation of the adrenal medulla in the cat.

Stimulation of the locus coeruleus in 40 cats leads to generalized activation of the sympathetic nervous system characterized by an immediate pressor response which was followed in the post-stimulus period by an increase of 49 +/- 10 and 44 +/- 6% in common carotid arterial resistance ipsilateral and contralateral to stimulation, respectively. This later response was not affected by vagotomy or bilateral cervical sympathectomy but was blocked by high spinal cord section. The post-stimulus carotid vasoconstrictor response could be entirely eliminated by acute bilateral physiological adrenalectomy in the form of adrenal hilar clamping, an effect which was reversible if the clamps were removed. The carotid vasoconstrictor response was associated with a rise in the circulating level of noradrenaline (260%) and adrenaline (196%), which was prevented by clamping the adrenal hilum. This response was not mediated via the hypothalamus because it persisted in the decerebrate animal, nor was it merely excitation of fibers of passage since it was reproduced by microinjection of glutamate into the locus coeruleus. The response was blocked by phentolamine suggesting it is mediated by alpha-adrenoceptors. These data represent the first conclusive demonstration that cell bodies in the brainstem are capable of activating the adrenal medulla. This fact is central to our present concept of the organization of the sympatho-adrenal axis.

Adrenal Medulla↗
PubMed1987

The involvement of the sympathetic nervous system in the centrogenic pressor and tachycardiac effects of prostaglandins E2 and F2 alpha in anaesthetised cats.

The intracerebroventricular (i.c.v.) administration of prostaglandin E2 (PGE2, 1 micrograms) and prostaglandin F2 alpha (PGF2 alpha, 10 micrograms) produced prolonged pressor and tachycardiac responses in chloralose-anaesthetised cats. Phenoxybenzamine-pretreatment completely prevented the pressor response without altering the tachycardiac response, whereas propranolol intervention completely inhibited the tachycardiac response and also attenuated the pressor response. The pretreatment with pentolinium completely antagonised both the pressor and tachycardiac responses to i.c.v. PGE2 and PGF2 alpha. The results suggest that the centrally administered PGE2 and PGF2 alpha augment sympathetic outflow to the heart and vascular system and thereby cause excitatory cardiovascular responses in anaesthetised cats.

Animals↗
PubMed1991

Hypothermia augments non-cholinergic neuronal bronchoconstriction in pithed guinea-pigs.

Electrical stimulation at C4-C7 in the spinal canal of pithed guinea-pigs injected with atropine, d-tubocurarine and pentolinium caused frequency-dependent bronchoconstriction. Such non-cholinergic responses to electrical stimulation, unlike responses to substance P, were abolished by pretreatment with capsaicin but not by mepyramine or propranolol. Bronchoconstrictor responses to electrical stimulation were inversely related to rectal temperature (between 30-40 degrees C) whereas responses to substance P increased with increasing temperature over the same range. Ouabain (i.v.) augmented responses to electrical stimulation at 35-37 degrees C but depressed those at 30-32 degrees C. Both morphine and the alpha 2-adrenoceptor agonist B-HT920 (i.v.) inhibited non-cholinergic-mediated bronchoconstrictor responses at 30-32 degrees C. These results stress the importance of adequate control of body temperature in this preparation. Lowered body temperature may increase neuronal output of neuropeptides whilst depressing bronchial smooth muscle sensitivity. The data support previous conclusions regarding the role of Na+/K+ activated ATPase in temperature-induced changes in sensitivity to bronchoconstrictor stimuli.

Adrenergic alpha-Agonists↗