Mechanism of the Immediate Capillary Stress Response

Abstract

Two possibilities may be considered for the mechanism of the immediate capillary stress response: the direct nervous origin, and the humoral. The latter was investigated in this study. Immediate capillary stress response was found in the absence of the adrenal, pituitary or thyroid glands, and after removal of both the adrenals and the pituitary. Among the 10 physiologic substances considered as playing a potential role in this phenomenon, three were found to possess capillary activity. Vasopressin as well as oxytocin increases capillary resistance. Histamine gives rise to a biphasic response, involving a decrease of capillary resistance (primary effect) followed by an increase (due to vasopressin elicited by histamine). By means of these substances it is possible to duplicate the immediate capillary stress response. During the immediate capillary response plasma has antidiuretic and chloruretic properties—a finding compatible with an increased vasopressin concentration and with the assumption that vasopressin is discharged rather regularly in the first phase of the stress response. The immediate capillary stress response seems to be the result of an interplay between vasopressin-oxytocin, and histamine. Species and individual differences in the sensitivity to these substances may account for the various patterns of the capillary response. The possible significance of the immediate capillary response and of the increased vasopressin activity in some clinical conditions is discussed.

FURTHER EVIDENCE FOR MEDIATION BY HISTAMINE OF ESTROGENIC STIMULATION OF THE RAT UTERUS12

“…Such a mechanism would explain the finding that cortisol when administered concurrently with estrogen did not prevent the estrogen-induced release of histamine, although it did eliminate the other measured responses to estrogen (1). These views are consistent with findings that vasodilation (26,27) and accompanying increase in capillary permeability (28,29) and other reactions resulting from histamine liberation or injection in extra-uterine tissues, can be diminished or prevented by the administration of cortisone-like adrenal steroids (28,(30)(31)(32)(33)(34)(35). Thus, cortisol appears to mimic the action of the effective antihistamines studied by antagonizing histamine at its site of action.…”