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Biomedical subjects

C J Pirola

Publications and source records attributed to C J Pirola.

45 records · Page 3Linked to original sources
PubMed1986

Saralasin blocks the effect of angiotensin II and extracellular fluid saline expansion on the Na-K-ATPase inhibitor release in rats.

A low molecular weight substance which behaves like ouabain as inhibitor of brain membrane Na-K-ATPase and 3H-ouabain binding was found in plasma after saline expansion of extracellular fluid or angiotensin II infusion into the third brain ventricle in the rat. Intracerebroventricular infusion of angiotensin II antagonist, saralasin, blocks the increase of the Na-K-ATPase inhibitor produced by infusion of angiotensin II into the third ventricle or extracellular fluid saline expansion.

Angiotensin II↗
PubMed1984

Increase in muscarinic receptors in rat intestine by thyrotropin releasing hormone (TRH).

The effect of Thyrotropin Releasing Hormone (TRH) on the contractile activity elicited by acetylcholine and electric stimulation in the rat ileus terminalis was investigated. TRH did not show any intrinsic contractile activity but, after a 30 minute latency period, the peptide caused a shift to the left of the dose-response curve for both acetylcholine and electric stimulation. The binding of 3H-quinuclidinylbenzilate (3H-QNB) assayed on ileum slices disclosed that the addition of TRH increased the number of muscarinic cholinergic receptors without changes in affinity when incubation was performed at pH 7.8, but no effect TRH was demonstrated at pH 7.4. Therefore, in spite of its neural and direct actions on intestine motor activity, TRH may affect the acetylcholine induced contraction by increasing the number of muscarinic receptors at a specific pH.

Acetylcholine↗
PubMed1984

Changes in plasma aldosterone levels and renin activity after bilateral superior cervical ganglionectomy in two strains of rats.

Superior cervical ganglionectomy (SCGx) of Wistar rats brought about a significant increase of plasma renin activity (PRA) 9 or 15 days later, an effect not observed 48 days after surgery. The same surgical procedure performed in Chbb Tom rats did not result in significant modification of PRA. In both strains of rats immobilization stress induced a 2.3-3.3-fold increase of PRA regardless of whether the animals had intact superior cervical ganglia. The injection of the angiotensin-converting enzyme inhibitor captopril to SCGx Wistar rats at the time of elevated PRA induced a severe hypotension, while it did not affect blood pressure in sham-operated animals. In both strains of rats SCGx resulted in depressed circulating aldosterone levels at all studied times after surgery.

Aldosterone↗
PubMed1983

Thyrotropin-releasing hormone increases the number of muscarinic receptors in the lateral septal area of the rat brain.

Stereotactic injection of acetylcholine (0.5-2 micrograms) into the lateral septal region of the rat brain produces a long-lasting sympathetic-mediated increase of the arterial blood pressure. This effect is mediated by muscarinic receptors since 1 microgram atropine abolishes this response. In this same brain region, TRH (0.5-4 micrograms) did not elicit any significant change in the arterial blood pressure, but potentiated the effect of acetylcholine. This phenomenon is apparently due to an increase of the number of muscarinic receptors in the lateral septal area of the rat brain.

Acetylcholine↗
PubMed1982

Circadian rhythm and neural regulation of rat pineal angiotensin converting enzyme.

Angiotensin converting enzyme was detectable in rat pineal gland and exhibited a circadian rhythm in activity with maximum at the end of the light phase of daily photoperiod. Superior cervical ganglionectomy (SCGx) or exposure to light for 6 days increased enzyme activity and obliterated morning-evening differences, whereas injection of the beta-agonist isoproterenol depressed the high values observed in SCGx animals. These results indicate that angiotensin converting enzyme in the pineal gland is under negative control by the norepinephrine released from pineal sympathetic nerves.

Animals↗
PubMed1978

Angiotensin regulates release and synthesis of serotonin in brain.

Angiotensin II released serotonin from neuron terminals and accelerated synthesis of the serotonin. This increase in synthesis depended on the activation of tryptophan hydroxylase. A biphasic effect was observed: at high doses the stimulatory effect depended on conversion of angiotensin II to angiotensin III. At low doses an inhibitory effect was found, possible dependent on an angiotensin II metabolite. These actions represent a subtle regulation of the open-loop serotonin system.

Angiotensin II↗
PubMedDate not supplied

Muscarinic M1 receptors in the lateral septal area mediate cardiovascular responses to cholinergic agonists and bradykinin: supersensitivity induced by chronic treatment with atropine.

The infusion of pilocarpine, acetylcholine, bradykinin and the selective M1 muscarinic agonist McNeil-A-343 into the lateral septal area produced a dose-dependent increase of arterial blood pressure and heart rate. The M1 muscarinic agonist carbamylcholine that causes a rise in arterial blood pressure when injected into the anterior lateral ventricles did not produce any cardiovascular effects when infused into the lateral septal area. Chronic treatment with atropine induced supersensitivity to the muscarinic agonists and a significant increase in the number of muscarinic receptors. In this study bradykinin failed to produce any significant change in cardiovascular activity. Pirenzepine, a M1 muscarinic blocking agent, inhibited completely the effect of both muscarinic agonists and bradykinin on cardiovascular activity. In fact, in vitro studies shows that the displacement of the binding of [3H]QNB by pirenzepine is compatible with the presence of the M1 subtype of muscarinic receptor in the lateral septal area, where it may play a major role on cardiovascular regulation.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗