Stimulation by Serotonin of Vasoactive Intestinal Polypeptide Release Into Rat Hypophysial Portal Blood

Shimatsu, Akira; Kato, Yuzuru; Matsushita, Norio; Katakami, Hideki; Yanaihara, Noboru; Imura, Hiroo

doi:10.1210/endo-111-1-338

Cited by 69 publications

(17 citation statements)

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“…VIP and OT are among the best-studied candidates for serotonin's downstream actions on PRL release (McCann et al, 1984;Shimatsu et al, 1982Shimatsu et al, , 1984Van de Kar et al, 1995). VIP and OT are both found in the PVN, implicating this structure as an important anatomic substrate of PRL release (Mezey and Kiss, 1985;Sofroniew et al, 1981;Swanson and Sawchenko, 1983).…”

Section: Modulatorsmentioning

confidence: 99%

“…VIP and OT are both found in the PVN, implicating this structure as an important anatomic substrate of PRL release (Mezey and Kiss, 1985;Sofroniew et al, 1981;Swanson and Sawchenko, 1983). Consequently, the PVN is among the best-studied sites of serotonininduced PRL release, and is known to contain the Recruitment of VIP neurons in the serotonin-induced PRL response is implied by the fact that VIP antiserum significantly blunts the usual PRL surge associated with serotonergic stimulation in vivo (Kaji et al, 1985;Shimatsu et al, 1982,). While it is hypothesized that VIP neurons of the PVN are directly stimulated by serotonergic fibers (Kiss et al, 1984;Lam, 1991;Reichlin, 1988), to date, serotonergic terminals have not been demonstrated on these VIPexpressing cells (Kiss et al, 1984).…”

Section: Modulatorsmentioning

confidence: 99%

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From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Emiliano

Fudge

2004

Neuropsychopharmacol

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The widespread use of the selective serotonin reuptake inhibitors (SSRIs) has been accompanied by numerous reports describing a potential association with hyperprolactinemia. Antipsychotics are commonly known to elevate serum prolactin (PRL) through blockade of dopamine receptors in the pituitary. However, there is little awareness of the mechanisms by which SSRIs stimulate PRL release. Hyperprolactinemia may result in overt symptoms such as galactorrhea, which may be accompanied by impaired fertility. Long-term clinical sequelae include decreased bone density and the possibility of an increased risk of breast cancer. Through literature review, we explore the possible pathways involved in serotonin-induced PRL release. While the classic mechanism of antipsychotic-induced hyperprolactinemia directly involves dopamine cells in the tuberoinfundibular pathway, SSRIs may act on this system indirectly through GABAergic neurons. Alternate pathways involve serotonin stimulation of vasoactive intestinal peptide (VIP) and oxytocin (OT) release. We conclude with a comprehensive review of clinical sequelae associated with hyperprolactinemia, and the potential role of SSRIs in this phenomenon.

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Section: Modulatorsmentioning

confidence: 99%

Section: Modulatorsmentioning

confidence: 99%

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Emiliano

Fudge

2004

Neuropsychopharmacol

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“…Numerous studies have examined the effects of many compounds on PRL secretion using urethane-anesthetized male rats [13,15,20,21] . Findell et al [7] postulated that urethane increases hypothalamic dopaminergic activity and that diminished PRL releease results from the increased levels of dopmine delivered to the anterior pituitary via hypophyseal portal blood vessels.…”

Section: Discussionmentioning

confidence: 99%

“…The effect of many compounds on PRL secretion has been examined in urethaneanesthetized male rats [15,20,22]. Urethane anesthesia results in a stabilization of plasma PRL levels lasting 2 hours after administration [16].…”

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confidence: 99%

Suppression of the Proestrus Prolactin Surge in the Rat Estrous Cycle by Urethane Anesthesia

Furudate

Nakano

1990

Experimental Animals

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“…71 At the same time, VIP release is stimulated by neostigmine 72 and by serotonin. 73 Certain potential physiological roles of cardiovascular peptides are suggested by the data presented above on their localization and actions. These roles include the regulation of regional blood flow, peripheral vascular resistance, and arterial blood pressure; and the regulation of cardiac function, including coronary blood flow, myocardial contractility, cardiac rhythmicity, and conductivity.…”

Section: Physiological Rolementioning

confidence: 98%

Vasoactive peptides. State-of-the-art review.

Said¹

1983

Hypertension

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SUMMARY At least 16 naturally occurring peptides either constrict or dilate blood vessels. Many of these peptides are present in nerve cells and nerve terminals supplying systemic and pulmonary blood vessels and the heart. Such neuropeptides are released locally as neurotransmitters, and can influence vascular tone, local and regional blood flow, arterial blood pressure, and cardiac function. There is evidence for the participation of at least some vasoactive peptides in the regulation of these functions and in the mediation or modulation of systemic shock and arterial hypertension. The investigation of vasoactive peptides in relation to cardiovascular function and dysfunction is at a promising threshold. There is a growing conviction that these peptides participate in the regulation of many organ functions. Neuroscientists, endocrinologists, and gastroenterologists have led other groups in recognizing the likely physiological and clinical significance of these peptides, most of which are found in the brain and gut.1 " 1 Since many biologically active peptides are capable of influencing vascular smooth muscle, and thus blood flow and blood pressure, peptides with these vasoactive properties are reviewed here. Emphasis is placed on the cardiovascular effects of the more recently identified peptides, with special reference to their possible roles in the regulation of blood pressure in normal and abnormal states. Bradykinin and angiotensins, which are extensively reviewed elsewhere, are only briefly mentioned here. Biological Activity of PeptidesWhich Peptides are Vasoactive?Peptides with vasoactive properties are given in the accompanying list (see box), which is not meant to be complete. For some of these peptides (e.g., angiotensin II, bradykinin), vasoactivity is a dominant feature of their biological actions; for others (e.g., prolactin, parathyroid hormone), the pressor or vasodepressor activity has generally been overshadowed by other actions of the peptide.As will become apparent in the following para : graphs, the ability to induce either vasodilation or vasoconstriction is shared by a variety of apparently unrelated peptides. It is possible in some instances, however, t o ' recognize certain structural features among these peptides that correlate with their vasodilator or vasoconstrictor activity. Such features will be noted. AngiotensinsAngiotensin II (table 1) is one of the most potent systemic vasopressors known. Its formation from angiotensin I through the action of angiotensin-converting enzyme, the localization and properties of this enzyme, and the physiology, pathophysiology, and pharmacology of the renin-angiotensin systems in the body are topics of recent comprehensive reviews.5 "" Bombesin A 14-residue peptide (table 1) isolated from the skin of the frog Bombina bombina, bombesin has spasmogenic activity on a variety of vascular and non-vascular smooth muscle structures.12 It induces vasoconstriction and systemic hypertension in most animal species, hypotension in monkeys, but neither in humans...

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Stimulation by Serotonin of Vasoactive Intestinal Polypeptide Release Into Rat Hypophysial Portal Blood

Cited by 69 publications

References 0 publications

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Suppression of the Proestrus Prolactin Surge in the Rat Estrous Cycle by Urethane Anesthesia

Vasoactive peptides. State-of-the-art review.

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