Biomedical subjects

V F Akins

Publications and source records attributed to V F Akins.

3 recordsLinked to original sources

PubMed1993

Hypothalamic histamine release, neuroendocrine and cardiovascular responses during tuberomammillary nucleus stimulation in the conscious rat.

Neuronal histamine (HA) in the central nervous system (CNS) has been implicated in control of peripheral cardiovascular and neuroendocrine responses. The tuberomammillary nucleus (TMN) of the posterior hypothalamus contains all CNS HA cell bodies. In these experiments, the TMN was electrically stimulated in conscious rats and HA release in the region of the supraoptic nucleus (SON) was estimated using in vivo microdialysis. In addition, mean arterial blood pressure (MAP), heart rate (HR), and plasma concentrations of norepinephrine (NE) and vasopressin (VP) were measured before, during and following TMN stimulation. Stimulation of the TMN resulted in a significant increase in extracellular HA (110 +/- 29% control) in the region of the SON. MAP, HR and plasma NE concentration were also significantly elevated during TMN stimulation. However, plasma VP concentrations were unchanged. These results show that TMN stimulation in conscious animals releases HA in the region of the SON and is associated with a pressor response, tachycardia, and increased plasma concentration of NE, but not release of VP.

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PubMed1991

Central nervous system histamine regulates peripheral sympathetic activity.

Brain histamine (HA) was depleted in conscious Sprague-Dawley rats by central administration of alpha-fluoromethyl-histidine (alpha-FMH), an irreversible inhibitor of the HA synthesizing enzyme. Isotonic or hypertonic saline was infused intravenously at 10 microliters.100 g-1.min-1 for 30 min and mean arterial pressure (MAP) and heart rate (HR) were monitored. In addition, plasma vasopressin (AVP) and norepinephrine (NE) were measured pre- and postinfusion. Animals pretreated with alpha-FMH showed a delayed and attenuated pressor response and bradycardia during hypertonic saline (HTS) infusion and a significant reduction in plasma NE levels (-29 +/- 8% below control values). However, plasma concentrations of AVP were similar in both groups. Central pretreatment with the H1-antagonist pyrilamine (PYR) also delayed the onset and significantly attenuated the pressor response to HTS infusion, and caused dose-related decreases in plasma NE concentrations (-34 +/- 8, -47 +/- 5, and -52 +/- 7% after 60, 100, and 600 nmol PYR, respectively). These data indicate a role for central HA in peripheral sympathetic activation but not as a mediator of AVP release to a peripheral hyperosmotic stimulus.

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PubMed1990

Brain histamine regulates pressor responses to peripheral hyperosmolality.

The role of brain histamine (HA) in the pressor response to peripheral hyperosmolality was investigated in the conscious Sprague-Dawley rat. Increased mean arterial pressure was observed during a 30-min intravenous infusion of hypertonic saline (HTS; 10 microliters.100 g body wt-1 x min-1) in vehicle-treated controls (20.1 +/- 3.8 mmHg) and in animals centrally pretreated with the specific H2-antagonist, cimetidine (15.0 +/- 3.7 mmHg). However, this pressor response was abolished in a dose-dependent manner after intracerebroventricular injection of the H1 antagonist promethazine. In other experiments, brain tissue microdissected from the supraoptic nucleus (SON), paraventricular nucleus (PVN), and posterior hypothalamic region showed significantly lower levels of total tissue HA after 60 min of intravenous HTS infusion compared with tissue taken from control animals receiving an isotonic infusion. Microdialysis in the region of the PVN or SON before and during HTS infusion showed increased extracellular concentrations of HA in the SON (24.4 +/- 10.9%) during infusion. No change in extracellular HA concentration was seen in the PVN during HTS infusion. These results support the conclusion that endogenous brain HA is involved in the pressor response to peripheral hyperosmolality.

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