PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PENTOLINIUM TARTRATE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1983

Intestinal fluid absorption in spontaneously hypertensive rats.

A comparison has been made of intestinal fluid absorption between male Okamoto spontaneously hypertensive rats (s.h.r.) and normotensive male Wistar controls. S.h.r. show enhanced fluid absorption both in hypertensive adults and in young s.h.r. before hypertension has developed. Several potential causes for increased fluid transport in s.h.r. were tested using pharmacological antagonists. It is unlikely that enhanced fluid absorption is due to high sympathetic nervous activity, the renin-angiotensin system or is secondary to hypertension. Intestine from s.h.r. have a high short-circuit current indicating a change in ion pump activity. These results are discussed in relation to the possible causes of increased fluid (ion) transport by the intestine of s.h.r.

Animals↗
PubMed1983

Neural control of periodic secretion of the pancreas and the stomach in fasting dogs.

The role of nerves in periodic secretion of the pancreas and the stomach in relation to the motility of the upper gastrointestinal tract was studied in conscious fasting dogs which had previously been provided with chronic gastric and pancreatic fistulae and a Heidenhain pouch. Both atropine and pentolinium abolished the periodic increase in gastric and pancreatic secretion and motility of the gut. Bilateral cervical vagal blockade with lidocaine reduced the motility of the stomach, the duodenum and the pouch preceding their peaks, but the motility at the peaks remained unchanged except in the case of the stomach. Pancreatic secretion preceding its peak was also decreased by vagal blockade but that at the peak was not significantly different from the control peak. Periodic pepsin secretion, from both the fistula and pouch, was decreased by vagal blockade. It is concluded that the secretion and motility of the upper gut in fasting dogs is controlled by periodic activity of the vagus and intrinsic nerves.

Animals↗
PubMed1984

Vagal control of gall-bladder contraction.

The role of the vagi in gall-bladder contraction was studied in conscious dogs with chronic biliary fistulae. The interdigestive periodic contraction of this organ was abolished by bilateral cervical vagal blockade, atropine or pentolinium, but neither methacholine nor carbachol initiated contraction when the duodenum was kept alkaline. The orthodox view that gall-bladder evacuation is primarily controlled by humoral mechanisms needs re-evaluation. Vagal blockade prevented the usual gall-bladder contraction in response to duodenal acidification.

Animals↗
PubMed1971

Acute controlled hypotension and EEG in patients with hypertension and cerebrovascular disease.

Forty-seven patients with hypertension and/or cerebrovascular disease were examined by an acute controlled hypotension test. This was performed by intravenous administration of the ganglionic blocking agent pentholonium and head-up tilting on a pivoted table with observation of the clinical neurological state and simultaneous EEG recording. Blood pressure was reduced by approximately 55% and brought to the point where signs of general cerebral ischaemia developed. By tilting back to horizontal the blood pressure returned to near the normal level. No change in focal neurological symptoms or changes in the EEG were observed, and it is concluded that the majority of hypertensive patients with or without previous stroke do tolerate normalization of their blood pressure. Controlled hypotension with tilting seems a simple and valuable test for excluding those few subjects who might not tolerate a blood pressure reduction. Whether EEG monitoring during the test increases the value of the test has not been answered.

Adult↗
PubMed1975

Relative influence of carotid baroreceptors and muscle receptors in the control of renal and hindlimb circulations.

In vagotomized dogs, a comparison was made of the relative ability of the carotid baroreceptors and of the receptors in skeletal muscles to cause constriction of the renal and hindlimb resistance vessels. With kidney and hindlimb perfused at constant pressure a decrease in pressure in the carotid sinuses from 250 to 40-45 mm Hg (1 mm Hg = 133 N/m2) caused the respective blood flows to increase by 19 +/- 6% and 80 +/- 4% (mean +/- SE), and stimulating muscle receptors with capsaicin caused a further decrease of 49 +/- 9% and 4 +/- 2%, respectively. With perfusion at constant flow, the baroreflex caused an increase of 34 +/- 4 mm Hg in the renal perfusion pressure and of 99 +/- 10 mm Hg in the hindlimb; capsaicin caused further increases of 203 +/- 17 and 35 +/- 9 mm Hg; respectively. These responses were abolished by sympathectomy. Capsaicin injection increased mean renal sympathetic nerve activity by 111 +/- 16% over the maximal impulse frequency recorded when the carotid sinus pressure was 40-45 mm Hg. Thus, withdrawal of the restraint exerted by the carotid baroreceptors on the pool of central neurons controlling the vascular beds of the hindlimb and kidney leads to near maximal constriction of the resistance vessels in the former bu not the latter; with strong activation of muscle receptors, near maximal constriction occurs in both beds.

Animals↗
PubMed1982

Liver glycogen synthase and phosphorylase changes in vivo with hypoxia and anesthetics.

Methods for obtaining and processing rat liver for determination of glycogen phosphorylase a and synthase I activity were studied. An extremely rapid and profound increase in phosphorylase was induced by hypoxia. The effect on synthase I was slower and less striking. Using alpha- and beta-adrenergic antagonists, a catecholamine-depleting agent, and a ganglionic blocking agent, it was determined that adrenergic stimulation secondary to the surgical procedure required to obtain the liver was not a significant factor. The anesthetic agent used also had a significant effect on the proportion of phosphorylase in the a form. Seconal anesthesia resulted in lower phosphorylase a levels than did ether or urethan anesthesia.

Anesthesia↗
PubMed1984

Differential effect of vasopressin on angiotensin and norepinephrine pressor action in rats.

The effect of vasopressin infusion on the pressor dose responses to angiotensin II and norepinephrine was studied in pentobarbital-anesthetized and unanesthetized nephrectomized rats. Pressor vasopressin (2-15 ng X kg-1 X min-1) given to anesthetized rats decreased sensitivity to angiotensin II in a dose-dependent manner (r = 0.88), an effect completely reversible by dPMeTyrAVP, a vasopressin vascular antagonist. Subpressor vasopressin (0.5-1 ng X kg-1 X min-1) given to unanesthetized rats diminished sensitivity to angiotensin II in the presence or absence of pentolinium (10 mg/kg). Shifts in dose-response curves to angiotensin II were always parallel. In contrast, dose responses to norepinephrine were not modified by vasopressin in pentolinium-treated rats and showed a small nonparallel rightward shift in animals without pentolinium. In animals without pentolinium, the baroreflex-mediated reduction in heart rate elicited by angiotensin II was not altered by vasopressin infusion. Our data suggest that vasopressin reduces angiotensin II pressor action by diminishing pressor sensitivity to the peptide. They indicate that the effect may be specific, mediated through the vascular receptor for vasopressin and independent of actions of this hormone on the autonomic nervous system.

Angiotensin II↗
PubMed1985

Reflexes fail to reduce pressor activity of vasopressin in spontaneous hypertension.

Pressor responses and heart rate responses were recorded in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto (WKY) rats during intravenous infusions of arginine vasopressin and phenylephrine under two experimental situations, first when cardiovascular reflexes were impaired by pretreatment with a ganglionic blocking agent (pentolinium) and second, when reflexes remained intact. In rats with ganglia blocked, pressor responses of SHR to vasopressin or to phenylephrine were similar to those of WKY rats. In rats with intact reflexes, pressor responses of SHR to phenylephrine were also similar to those of WKY rats but, in contrast, pressor responses of SHR to vasopressin were enhanced. Heart rate fell much more for any given elevation of blood pressure in WKY rats than in SHR during infusions of vasopressin and phenylephrine, and the bradycardia associated with these pressor agents was largely abolished by pentolinium. The results are consistent with the hypothesis that baroreflexes buffer the pressor activity of vasopressin in the normotensive WKY rat and that an impairment of baroreflex activity in SHR contributes to the enhanced pressor activity of vasopressin in these rats.

Animals↗
PubMed1986

Sympathomimetic pressor responses to thyrotropin-releasing hormone in rats.

Cardiovascular responses to centrally administered thyrotropin-releasing hormone (TRH) were studied in urethan-anesthetized rats to allow continuous recording of attendant changes in sympathetic nerve activity. Intracerebroventricular infusions of TRH (0.05-5.0 micrograms) consistently increased not only blood pressure and heart rate, but also spike frequency in splanchnic, renal, or cervical sympathetic nerves. Parasympathetic inhibition seemed unlikely because TRH responses were unaltered by cholinergic blockade with atropine, and efferent vagal nerve firing, instead of being reduced, was actually increased by TRH. An increased secretion of endogenous vasopressin also appeared unlikely, since TRH responses were essentially unaffected by either hypophysectomy or pretreatment with a vasopressin antagonist. Inasmuch as pharmacological ganglion blockade with pentolinium eliminated increases in splanchnic nerve firing but reduced the attendant tachycardia by only 50%, residual tachycardia after ganglion blockade was considered partly due to persistent sympathetic cardioaccelerator tone. On the other hand, because pressor responses to TRH were always accompanied by increased sympathetic nerve firing and were completely abolished after pentolinium-induced ganglioplegia, they were attributed solely to sympathetic hyperactivity.

Animals↗
PubMed1989

Mechanism of pressor response to posterior hypothalamic injection of neuropeptide Y.

Unilateral microinjection of neuropeptide Y (NPY) into the posterior hypothalamic nucleus was previously found to evoke an increase in mean arterial pressure (MAP) in urethan-anesthetized rats. In this study, the mechanism by which this increase occurs was examined. Pretreatment of rats with 2.0 mg/kg (iv) of phenoxybenzamine, or 7.5 mg/kg (iv) of pentolinium, resulted in a significant reduction in the peak MAP evoked by microinjection of NPY (2.35 nmol) into the posterior hypothalamic nucleus. Administration of the vasopressin V1-receptor antagonist [d(CH2)5Tyr(Me)]AVP (10 micrograms/kg iv) before microinjection of NPY failed to attenuate the increase in MAP. Similar results were obtained with respect to the effect of these three antagonists on the increase in MAP evoked by injection of the cholinergic muscarinic agonist carbachol (5.48 nmol) into the posterior hypothalamic nucleus. Furthermore, microinjection of NPY or carbachol elicited a significant elevation of renal sympathetic nerve activity and an increase in resistance of the hindquarter vascular bed. However, NPY elicited a decrease and carbachol an increase in the resistance of the mesenteric bed, whereas NPY elicited an increase and carbachol a decrease in the resistance of the renal bed. These results suggest that NPY elicits an increase in MAP via centrally mediated sympathetic excitation. Furthermore, NPY and carbachol differentially affect sympathetic outflow to peripheral vascular beds after microinjection into the posterior hypothalamic nucleus.

Animals↗
PubMed1989

Regional hemodynamic and baroreflex effects of endothelin in rats.

Endothelin is a peptide with potent, long-lasting pressor effects characterized by increases in mesenteric and hindquarters vascular resistance and bradycardia following an initial, transient depressor response. This study examined the mechanisms of action of endothelin on regional hemodynamics in conscious, freely moving rats and on baroreflex sensitivity both in conscious and chloralose-anesthetized rats. The pressor response to endothelin (0.67 nmol/kg) was attenuated by nifedipine (25 micrograms/kg) and augmented by chloralose anesthesia. The bradycardia was attenuated by pentolinium (10 mg/kg), atropine methyl sulfate (0.5 mg/kg), or chloralose anesthesia. Hindquarter vaso-constriction was attenuated by nifedipine, pentolinium, and atropine, whereas mesenteric vasoconstriction was less sensitive to blockade. The vasopressin V1 antagonist, [d(CH2)5Tyr(Me)]-AVP (20 micrograms/kg), indomethacin (5 mg/kg), or verapamil (150 micrograms/kg) did not affect any of these cardiovascular responses. Renal sympathetic nerve activity was reduced similarly in chloralose-anesthetized rats to pressor responses elicited by either phenylephrine or endothelin, and the slope of the baro-reflex function curve after endothelin was similar to that of phenylephrine. These results suggest that endothelin is a potent vasoconstrictor in which its action on visceral and skeletal muscle vasculature is mediated by somewhat different mechanisms. Endothelin does not alter baroreceptor reflex control of sympathetic nerve activity or heart rate.

Animals↗
PubMed1991

Regional blood flow effects of ANP in conscious dogs: preferential gastrointestinal vasoconstriction.

We studied total and regional blood flow responses to human atrial natriuretic peptide (alpha-hANP) using radioactive microspheres in six conscious dogs. Hemodynamic responses to infusions of alpha-hANP at 75 ng.kg-1.min-1 were determined in each dog in the presence and absence of autonomic reflexes using the ganglion blocking agent pentolinium. When autonomic reflexes were blocked, alpha-hANP caused a substantial reduction in gastrointestinal (GI) vascular conductance (35%) but had no significant effects in brain, kidneys, liver, skeletal muscle, or skin. This alpha-hANP-induced fall in GI conductance contributed more than 40% to the fall in total peripheral conductance (TPC) of 24% occurring after autonomic blockade. A fall in myocardial vascular conductance, most prominent in the left ventricle, contributed a further 40% to the fall in TPC. When autonomic reflexes were intact, alpha-hANP caused vasoconstriction in the GI region (29% fall in vascular conductance), had no significant effects on myocardial vascular conductance but significantly increased splenic vascular conductance. In addition to these systemic responses, alpha-hANP infusion also significantly reduced pulmonary vascular conductance, independent of autonomic reflex activity or changes in pulmonary artery pressure. Thus our results in conscious dogs demonstrate that alpha-hANP causes a systemic vasoconstriction, most pronounced in the GI region.

Animals↗
PubMed1997

Separation of peripheral and central cardiovascular actions of angiotensin II.

The pressor and vasoconstrictor action of angiotensin II (ANG II) is considered to be caused by a combination of its direct and indirect vascular effects, the latter mediated by the sympathetic nervous system. The purpose of this study was to determine the extent to which the direct and indirect actions of ANG II contribute to its pressor and vascular effects. Blood pressure, cutaneous vascular, and plasma norepinephrine responses to intravenous ANG II were measured in conscious rabbits before and after inhibition of central sympathetic outflow with intravenous and intracisternal clonidine and after ganglionic blockade with intravenous pentolinium. Intravenous ANG II caused a similar dose-related rise in blood pressure before and after sympathetic blockade with intravenous clonidine, intracisternal clonidine, and intravenous pentolinium. In contrast, the dose-related fall in cutaneous ear blood flow and cutaneous ear temperature and rise in cutaneous ear vascular resistance induced by intravenous ANG II were abolished after intravenous clonidine, intracisternal clonidine, and intravenous pentolinium. Heart rate was unchanged after ANG II. There were no changes in back skin or rectal temperature. There was a nonsignificant fall in plasma norepinephrine and no change in epinephrine after ANG II. These results demonstrate that the acute pressor response to intravenous ANG II is mediated by its direct vascular effects and is not dependent on central or ganglionic stimulation of the sympathetic nervous system, in contrast to the effect of ANG II on cutaneous ear vasoconstriction, which is predominantly caused by a centrally mediated increase in sympathetic nervous activity. Our results separate, in conscious rabbits, the direct vascular effects of ANG II from its indirect vascular actions, which are mediated by central sympathetic stimulation in the brain.

Angiotensin II↗