Contractile effects of perivascularly applied vasopressin on the pial artery of the cat brain.

Abstract

SUMMARY1. The effects of perivascularly applied vasopressin on the diameter of pial arteries (control 298 + 14 S.E. ,m) of the brain were examined after chronic implantation of a cranial window in fifteen anaesthetized cats.2. Application of vasopressin resulted in a dose-dependent contraction. The threshold concentration for contraction was 3 x 10-10 M, the half-maximal effective concentration (ED50) (16±+02) x 10-9 M, and the maximum reduction in artery diameter 37 + 2 /.3. The contraction was powerfully inhibited by perivascular application of a 10-M solution of the vasopressin antagonist, [1-(,8-mercapto-,8,,8-cyclopenta-methylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin. 4. Perivascular application ofnoradrenaline induced a dose-dependent contraction of the pial artery. The ED50 was (8-9 + 2 5) x 10-7 M, and the maximum reduction in artery diameter was 33 + 2 %.5. Such noradrenaline-induced contraction was not modified at all in the presence of a subthreshold dose (2 x 10-10 M) of vasopressin (P > 0 05, for the over-all difference in size of the contraction, ED50 and maximum contraction).6. In another experimental setting it was also found that neither the subthreshold nor a suprathreshold (10-9 M) dose of vasopressin modified the contraction induced by 10-6 M-noradrenaline (P > 0 05, compared to the contraction in the absence of vasopressin).7. Thus a powerful and sensitive contractile response of the pial arteries to perivascularly applied vasopressin was demonstrated. However, the modifying effect of vasopressin on the contraction induced by perivascularly applied noradrenaline was minimal.

Cerebral vasoconstriction produced by vasopressin in conscious goats: role of vasopressin V1 and V2 receptors and nitric oxide

“…The present results under control conditions con®rm previous observations using the same experimental preparation (Lluch et al, 1984), and show that arginine vasopressin produces cerebral vasoconstriction as also occurs in cerebral vessels from dierent species, including humans (Lluch et al, 1984;Nakai, 1987;Faraci et al, 1988;Onoue et al, 1994). Nevertheless, although most of the studies may show that arginine vasopressin produces cerebral vasoconstriction, there are also studies showing that this peptide can produce cerebral vasodilatation (Katusic et al, 1984;Suzuki et al, 1992;Onoue et al, 1994).…”

“…In the cerebral circulation, most of the studies show that arginine vasopressin produces vasoconstriction in dierent species, including humans (Lluch et al, 1984;Nakai, 1987;Faraci et al, 1988;Onoue et al, 1994), and it has been reported that the magnitude and the sensitivity of the constriction of pial arteries in response to this peptide are higher than those exhibited by coronary, renal, saphenous, mesenteric and pulmonary arteries from rabbits (Garcõ aVillalo n et al, 1996). These studies, together with observations showing that concentrations of arginine vasopressin in cerebrospinal¯uid are higher than in plasma (Luerssen et al, 1977), and that this peptide has been identi®ed by immunoreactive procedures in cerebral arteries and veins (Feuerstein & Miller, 1997), suggest that arginine vasopressin may play a role in the regulation of the cerebral circulation.…”

Triphasic Response of Rat Intracerebral Arterioles to Increasing Concentrations of Vasopressin in vitro

“…Vasopressin has been reported to be both a vasoconstrictor (Lluch et aI. , 1984;Nakai, 1987;Martin de Aguilera et aI. , 1990;Fugii et aI.…”

Role of Vasopressin V1a and V2 Receptors for the Development of Secondary Brain Damage after Traumatic Brain Injury in Mice

“…Another possible mechanism is the direct influence of vasopressin on the diameter of cerebral blood vessels. Several studies showed that AVP induces cerebral vasoconstriction in different regions of the normal rodent and human brain (Nakai, 1987;Faraci et al, 1988;Onoue et al, 1994;Fernandez et al, 2001), an effect mediated by AVP V 1 receptors (Martin et al, 1990;Garcia-Villalon et al, 1996;Fernandez et al, 2001). In the injured brain, AVP-mediated vasoconstriction may result in reduced pericontusional=pen-penumbral blood flow, finally leading to enhanced tissue damage and brain edema formation.…”