Description:
<jats:p>Our recent data suggest that spontaneously hypertensive rats (SHR) show reduced functional hyperemia and impaired relaxation of vertebral and basilar arteries. Here, using brainstem slices from pre‐hypertensive SHR (PHSHR, P21‐P30), young hypertensive SHR (YHSHR, P45‐P70) and age‐matched normotensive Wistar rats, we compared vascular dilatory capacity of both pial and penetrating parenchymal arterioles. Changes in vascular diameter in response to application of vasodilator agents, adenosine (1‐10 µM) and sodium nitroprusside (1‐10 µM), were assessed after pre‐constriction with a thromboxane agonist (U46619 70 nM). In PHSHR and aged‐matched Wistar rats, treatment with U46619 constricted parenchymal arterioles to 82±7% and 88±2% of their resting diameters: 15±3μm and 16±2μm, respectively. These responses remained unchanged in YHSHR and their aged‐matched controls. Adenosine reversed the U46619‐induced vasoconstriction by 24% and 30% in PHSHR and Wistar controls, respectively. In contrast, adenosine failed to reduce vasoconstriction in YHSHR, although its vasodilator efficiency in aged‐matched Wistar rats remained unaltered. Likewise, superfusion with sodium nitroprusside reduced the U46619‐induced vasoconstriction in penetrating arterioles from PHSHR, but not YHSHR. Intriguingly, vasodilator efficiency of adenosine in pial arterioles of a similar size (21±4 μm) was preserved in YHSHR. These results suggest that the dilatory capacity of brainstem parenchymal arteries is reduced in YHSHR. Whether this contributes to neurogenic hypertension remains to be determined. The distinct responses of parenchymal versus pial arterioles in YHSHR suggest that the impaired dilatory reserve cannot be ascribed to increased blood pressure <jats:italic>per se</jats:italic>. BHF funded research.</jats:p>