Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of intracerebroventricular (icv) administration of somatostatin(1-14) (SS1-14) on mean arterial blood pressure (MAP), heart rate (HR), plasma arginine vasopressin (AVP) concentration, and splanchnic nerve activity (SpNA) were studied in conscious rats. In addition, the effects of peripheral alpha-adrenergic receptor blockade with prazosin, vasopressinergic V1-receptor blockade with [d(CH2)5Tyr(Me)]AVP, and chronic bilateral sinoaortic denervation (SAD) on central SS1-14-induced MAP, HR, and SpNA responses were investigated. SS1-14 icv elicited dose-dependent increases in MAP and plasma AVP concentration as well as decreases in HR and SpNA. Prazosin iv did not significantly affect SS1-14-induced pressor and bradycardic responses but augmented the decrease in SpNA. The V1-AVP receptor antagonist iv significantly attenuated the effects of SS1-14 icv on MAP, HR, and SpNA. Following SAD the pressor responses to SS1-14 icv were significantly enhanced and were associated with significantly smaller decreases in HR and SpNA. We conclude that central administration of SS1-14 causes a pressor response via release of AVP while at the same time inhibiting peripheral sympathetic outflow. Our results support the hypothesis that SS1-14 in the brain by its effects on AVP release and sympathetic outflow may participate in central cardiovascular regulation.
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PMID:Central effects of somatostatin: pressor response, AVP release, and sympathoinhibition. 257 3

The effects of somatostatin on plasma concentrations of insulin and glucose in the presence of the selective alpha 1-adrenoceptor blocking agent prazosin or the selective alpha 2-adrenoceptor blocking drug yohimbine were studied in vivo in anesthetized rats. Infusion of both prazosin (0.080 mg/min) and yohimbine (0.018 mg/min) increased plasma insulin levels within 10 min. Prazosin, but not yohimbine, caused a significant increment in plasma glucose concentrations during the infusion of both prazosin and yohimbine, suggesting that the inhibitory effect of somatostatin is not mediated via a direct action on alpha 1- or alpha 2-adrenoceptors. Plasma glucose concentration fell slightly during somatostatin administration. A marked increment in insulin release occurred in response to cessation of the somatostatin infusion, both during prazosin- and yohimbine-treatment. We conclude that somatostatin efficiently inhibits insulin secretion during selective alpha 1- and alpha 2-adrenoceptor blockade and, further, that the insulin off-response after somatostatin treatment is potentiated by alpha-adrenoceptor blockade. This study also indicates that blockade of alpha 1- as well as alpha 2-adrenoceptors leads to an increased insulin secretion.
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PMID:Enhancement of insulin secretion during selective blockade of alpha 1- and alpha 2-adrenoceptors in the rat: effects of somatostatin. 612 72

The administration of an i.p. dose of phenylephrine (2 mg/kg) increased the number of [125I]Tyr11-somatostatin ([125I]Tyr11-SS) receptors and decreased their apparent affinity in rat hippocampal membranes 7 h after its injection. Prazosin (20 mg/kg, i.p.) administered 1 h before phenylephrine reversed effects of the latter on SS binding. Prazosin alone decreased the number of SS receptors without changing the affinity. The addition of phenylephrine or prazosin (10(-5) M) to the incubation medium did not change the SS binding characteristics. The present results support the notion that the alpha 1-adrenergic system regulates the binding of SS to its specific receptors in rat hippocampus.
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PMID:Changes in alpha 1-adrenergic neurotransmission alter the number of somatostatin receptors in the rat hippocampus. 752 2