ALTERATIONS IN THE OXYTOCIN-INDUCED INTRA-MAMMARY PRESSURE RESPONSE AFTER MECHANICAL STIMULATION OF THE MAMMARY-GLAND OF THE ANESTHETIZED LACTATING RAT

The hypothesis that 17β-estradiol suppresses dopamine secretion into hypophysial portal blood was tested. Portal plasma concentrations of dopamine were significantly lower in proestrous rats (1.0 ± 0.1 ng/ml; mean ± SE) than in estrous rats (1.9 ± 0.38 ng/ml). To deplete the animal of endogenous steroid hormones, proestrous rats were adrenalectomized (Adx) and ovariectomized (Ovx). Twenty-four hours later, hypophysial portal blood was collected for 60 min, and the plasma from this blood was analyzed for dopamine. Arterial plasma from these rats was assayed for 17β-estradiol and progesterone. The concentrations of dopamine in the portal plasma of sham-operated rats and bilaterally Adx-Ovx rats were similar to those in estrous animals. The concentration of dopamine in portal plasma of Adx-Ovx rats injected 24 h earlier with 50 μg 17β-estradiol was 1.0 ± 0.31 ng/ml, which was comparabExposure of adipocytes from young rats (2–3 months old) to dexamethasone in vitro results in 40–50% inhibition of glucose transport and metabolism. ComparabRhythmic, manual compression applied for 10–15 sec to two thoracic mammary glands of the urethane-anesthetized rat resulted in an immediate and significant reduction in amplitude of the intrammary pressure (IMP) response in abdominal glands induced by iv injected oxytocin. The period of reduced responsiveness to oxytocin lasted 13 min on the average; then the IMP responses gradually returned over the next few minutes to prestimulus heights. This invariably was followed by a phase of increased responsiveness to oxytocin lasting several minutes, during which the amplitude progressively increased to a maximum which was significantly above that seen before manual compression. A similar pattern of depression, recovery, and increased responsiveness of the IMP response to a given dose of oxytocin occurred if a single iv injection of 5 μg epinephrine was given instead of mammary compression. The IMP response was not reduced by manual compression of the thoracic glands if 1) the rat was pretreated with the β-adrenergic blocking drug, propranolol; 2) the glands to be compressed were first locally anesthetized with carbocaine; or 3) manual compression was applied during the phase of increased responsiveness induced earlier either by manual compression or epinephrine. These results indicate that the motor-inhibitory system of the rat mammary gland, which is composed mainly of sympathetic components, can be reflexly activated by mechanical stimulation of the mammary gland area. This mechanism may be responsible for the failure of rat pups to obtain significant quantities of milk during the first 10–15 min of suckling in the conscious rat. © 1979 by The Endocrine Society.