Elevated blood pressure after pinealectomy in the rat

Abstract

Previous observations have suggested a role for the pineal gland in regulation of blood pressure. To investigate this possibility, pinealectomy was performed in prepubertal (43-day-old) and postpubertal (55-day-old) male rats. Systolic blood pressure (BP) was measured by the tail cuff method in conscious pinealectomized (Px) and sham pinealectomized (ShPx) rats at various times. In the 3 weeks following surgery, the BP increase after Px was twice that after ShPx (p less than 0.05). During administration of 1% saline as the sole fluid source from day 96-123, hypertension (BP greater than 150 mmHg) was observed in those animals Px at day 43 (p less than 0.05 vs ShPx) but not in those Px on day 55. Moreover, saline consumption was increased in the hypertensive group compared to ShPx controls. There was no significant difference in mean body weight or heart rate between Px or ShPx groups. These data suggest that pinealectomy in the prepubertal period may result in a tendency to hypertension, measurable in conscious rats, which is unmasked by saline administration.

Pinealectomy Aggravates and Melatonin Administration Attenuates Brain Damage in Focal Ischemia

“…However, the arterial blood pressure and cerebral blood flow were not monitored in these pioneering studies. Although the antioxidant property of melatonin might account for its neuroprotective effect, monitoring cerebral blood flow is indispensable in pinealectomized rats because they may be hypertensive for the first 60 days after pinealectomy (Zanoboni et al, 1978; Vaughan et al, 1979) and also because melatonin has been reported to have a regulatory action on cerebral blood flow (Viswanathan et al, 1990, 1997; Mahle et al, 1997; Geary et al, 1997). We used rats that were pinealectomized 3 months before MCA occlusion to eliminate any possible action of pinealectomy-induced hypertension on stroke outcome (Zanoboni et al, 1978).…”

“…Pinealectomy leads to an increase in systemic arterial blood pressure (Karppanen et al, 1975; Zanoboni et al, 1978; Vaughan et al, 1979) in addition to a drastic reduction in circulating levels of melatonin (Ozaki and Lynch 1976; Lewy et al, 1980; Bubenik and Brown, 1997). Cerebral vessels express melatonin receptors (Viswanathan et al, 1990, 1997), and in vitro , melatonin has been shown to induce concentration-dependent vasoconstriction or dilation (Geary et al, 1997; Mahle et al, 1997).…”

Melatonin reduces disseminate neuronal death after mild focal ischemia in mice via inhibition of caspase‐3 and is suitable as an add‐on treatment to tissue‐plasminogen activator

“…Brain protection is independent of hemodynamic changes and involves inhibition of caspase-3. arterial blood pressure [19][20][21] and either constricts or dilates blood vessels in a concentration-dependent manner [22,23]. In transient focal ischemia, it was previously shown in rats that melatonin increases cerebral laser Doppler flow (LDF) after tissue reperfusion [6].…”

Prophylactic use of melatonin protects against focal cerebral ischemia in mice: role of endothelin converting enzyme‐1

“…In addition to its free radical scavenging actions, melatonin also exhibits pronounced vascular effects. Thus, melatonin reduces arterial blood pressure [10–13] and, depending on the dose and experimental condition, either constricts or dilates blood vessels [14, 15]. In the brain, melatonin increases cerebral blood flow (CBF) after focal ischemia [2] and also decreases the lower threshold of CBF autoregulation [16], suggesting stabilization of vascular function.…”