We demonstrated that cocaine or cold water stress (CWS) elicits systemic vasoconstriction
in Brown-Norway (BN) rats but an increase in cardiac output in Dahl salt sensitive
(DSS) rats. Since the DMH plays an important role in stress responsiveness, we sought
to determine the role of the DMH to these disparate stressors on regional vascular
hemodynamics. We hypothesized that inhibition of the DMH would attenuate greater hindquarters
vasoconstriction to either stress in BN compared to DSS rats. BN and DSS rats were
instrumented for determination of arterial pressure, heart rate, and with pulsed Doppler
flowprobes on the superior mesenteric and abdominal aorta. Bilateral guide cannulas
were implanted above the DMH. After recovery, we observed that cocaine (5 mg/kg, iv) elicited greater hindquarters and mesenteric vasoconstriction and greater
bradycardia in BN rats compared to DSS rats. In contrast, CWS (1 cm deep for 1 min) elicited tachycardia in all rats and greater increases in mesenteric resistance
in BN rats but hindquarters vasodilation that was greater in BN compared to DSS rats.
Therefore, visceral and skeletal muscle vascular responses differed between strains
and stressors. We examined the dependence of these responses on the DMH with bilateral
microinjections of muscimol (80 pmol in 100 nl) in the DMH. Muscimol attenuated the greater hindquarters and mesenteric vasoconstriction
and tachycardia in BN rats without affecting responses in DSS rats in response to
cocaine. Responses to CWS were unaffected by muscimol except that tachycardia was
selectively reduced in BN rats. Kainate (10 pmol) in the DMH elicited a similar response
pattern as CWS. These studies demonstrate that the DMH plays a strain- and stimulus-dependent
role in mediating hemodynamic responses to stress. Our data suggest that there are
significant variations in central neural pathways mediating stress that vary in different
rat strains.
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© 2010 Published by Elsevier Inc.