Cardiovascular effects of intracerebroventricularly administered growth hormone-releasing factor in spontaneously hypertensive rat.

Summary 1. We investigated the cardiovascular effects of intracerebroventricularly administered (ICV) growth hormone-releasing factor (GRF) in both spontaneously hypertensive rats (SHR) and Wistar rats (WR) with reference to the involvement of adrenergic mechanisms and plasma AVP concentration. 2. The ICV GRF induced biphasic changes of mean arterial pressure (MAP) in SHR. In the first phase, maximum pressor response was observed 2–3 min after injection. In the second phase, maximum depressor response was observed 12–13 min after injection, and lasted up to 21–22 min. In WRY there were no significant changes in MAP. 3. ICV phentolamine attenuated the GRF-induced pressor response, but did not affect the depressor response. ICV bunazosine had no effect in both responses. ICV yohimbine attenuated the GRF-induced pressor response, but did not affect the depressor response. 4. In SHR, plasma AVP concentration was not affected by ICV GRF. 5. These data suggest that central GRF plays an important role in the maintenance of hypertension in SHR, since ICV GRF caused a significant depressor effect in SHR but not in WR. ICV GRF induced biphasic changes of MAP in SHR. The pressor response was mediated through central α2-adreno-ceptors. The depressor response was not mediated through central α-adrenoceptors. The depressor effect of ICV GRF was not mediated by the changes of plasma AVP concentration.