Disease relevance of SSTR2

• It is concluded that SRIF may change the normal 5-deiodinase (5-D) activity and increased rT3 during hyperthyroxinemia into a 5'-D activity and a rise in T3, respectively, in T. nilotica [1].
• Atipamezole partially suppressed xylazine-induced hyperglycemia, but SRIF completely suppressed the hyperglycemia for the first 60 min after the xylazine injection and the suppression by SRIF was stronger than that by atipamezole [2].

High impact information on SSTR2

• Somatostatin (SRIF) is a putative peptide neurotransmitter that may interact with brain capillaries following neurosecretion of the peptide [3].
• The effect of SRIF was additive to that of thyroid hormones in suppressing the release of TSH and its subunits by TRH [4].
• A combination of SRIF and thyroid hormone completely suppressed the release of TSH and its subunits by TRH [4].
• Therefore, we postulate that octreotide exerts its effects mainly through binding to the SSTR2 [5].
• Our data show that estradiol and the androgens generated distinctly different patterns of GHRH and SRIF release, which in turn established gender-specific GH patterns [6].

Biological context of SSTR2

• These studies suggest that brain microvessels rapidly sequester and degrade SRIF analogues and that this may represent one mechanism for rapid inactivation of the neuropeptides subsequent to neurosecretion [3].
• These results suggest that GH regulation in avian species is partly mediated by an inhibitory short-loop mechanism (mediated by hypothalamic SRIF and a down-regulation of pituitary TRH-binding sites) that suppresses basal and secretagogue-induced GH release [7].
• Activation of D1 receptor with 10(-8) M and 10(-6) M SKF 38393 increased AUC for SRIF from 5.6 (control) to 420 and 500 +/- 57.8 ng.ml-1 min, but 10(-10) M SKF 38393 was ineffective [8].

Anatomical context of SSTR2

• SSTR2 was found in the hypothalamus, cerebrum, cerebellum, pituitary, stomach and testis [9].
• The effect of hypophysectomy and bovine GH administration on somatostatin (SRIF) content in the rat hypothalamus was investigated [10].
• In order to characterize the receptors mediating this action, we have tested several SP and SRIF analogues for their effects on release of [3H]L-norepinephrine ([3H]NE) from chromaffin cell cultures [11].
• Co-storage and co-secretion of somatostatin (SRIF) and catecholamine (CA) were demonstrated using bovine adrenal medulla [12].
• SRIF injection decreased plasma GH concentration in 270-day-old fetuses [13].

Associations of SSTR2 with chemical compounds

• Radioiodination of SSTR2 was performed by chloramin T method followed by purification of radioiodinated material on Sephadex G-25 column [9].
• These analogues were found to be active but less potent than SRIF in inhibiting nicotine-induced [3H]NE release from these cultures, suggesting that the site mediating this action differs in its structural requirements from the SRIF receptor found in some other tissues [11].
• Clonidine and guanabenz did not affect release of SRIF [14].
• If, however, SRIF was injected together with these hormones, which raised plasma T4, or together with T4 itself, an increase in plasma concentrations of T3 could be observed, whereas the increase in rT3 was less pronounced [1].
• In contrast, quinelorane, a D2 receptor agonist, and haloperidol, which blocks D2 receptors, did not affect release of SRIF or GHRH [8].

Analytical, diagnostic and therapeutic context of SSTR2

• OBJECTIVE: To develop radioimmunoassay for somatostatin receptor type 2 (SSTR2) and search for its presence in certain rat tissues [9].
• In summary, active immunization against SRIF in growing pigs increased ST and IGF-I concentrations [15].
• Immunization against SRIF had no effect on blood metabolites; however, GRF infusion increased free fatty acids from 157 to 204 microEq/l (SE = 11) and decreased blood urea nitrogen from 4.1 to 3.5 mmol/l (SE = 0.2) from day 1 to day 6, respectively [15].
• A series of five intravenous injections of 1 mg of SRIF at 10-min intervals also blunted xylazine-stimulated GH release [2].

References