Referenced in: none

Automatically associated channels: Kir2.3

Title: Direct coupling of the somatostatin receptor to potassium channels by a G protein.

Authors: A Yatani, L Birnbaumer, A M Brown

Journal, date & volume: Metab. Clin. Exp., 1990 Sep , 39, 91-5

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/2169576

Abstract
G proteins couple receptors to ionic channels indirectly by acting on membrane enzymes which modulate channel activity through second or third messengers such as cytoplasmic kinases, IP3 or Ca++. Recently, it has been shown that G proteins can act on ionic channels in a membrane-delimited or direct manner; from our experience this phenomenon seems to be widespread. A G protein purified from human red blood cells (hRBC) Gk when preactivated with GTP gamma S acts directly on muscarinic acetylcholine receptor-regulated K+ channels (K+[ACh]) in atrial cells and the stimulatory regulator of adenylyl cyclase, Gs from hRBCs acts directly on two distinct voltage-gated Ca++ channels, one in cardiac muscle and the other in skeletal muscle T-tubules. In many cells, including clonal GH3 pituitary cells, somatostatin (SST) inhibits secretion by a complex mechanism that involves a pertussis toxin (PTX)-sensitive step. This is not due to lowering cAMP since secretion induced by cAMP analogs and K+ depolarization are also inhibited. SST also causes membrane hyperpolarization, which is similar to the effect of ACh on cardiac pacemaking cells and may lead to decreases in intracellular Ca++ needed for secretion. ACh acting through a muscarinic recpetor in GH3 cells has the same effects as SST.(ABSTRACT TRUNCATED AT 250 WORDS)