Related Experiment Video
Updated: Apr 27, 2026

Isolation of Intrapulmonary Artery and Smooth Muscle Cells to Investigate Vascular Responses
Published on: June 8, 2022
Postischemic reperfusion causes smooth muscle calcium sensitization and vasoconstriction of parenchymal arterioles
Marilyn J Cipolla1, Siu-Lung Chan2, Julie Sweet2
1From the Department of Neurological Sciences (M.J.C., S.-L.C., J.S.), Department of Pharmacology (M.J.C., M.J.T., J.E.B.), and Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Vermont, Burlington (M.J.C., N.G.). Marilyn.Cipolla@uvm.edu.
Background And Purpose:
Parenchymal arterioles (PAs) are high-resistance vessels in the brain that connect pial vessels to the microcirculation. We previously showed that PAs have increased vasoconstriction after ischemia and reperfusion that could increase perfusion deficit. Here, we investigated underlying mechanisms by which early postischemic reperfusion causes increased vasoconstriction of PAs.
Methods:
Isolated and pressurized PAs from within the middle cerebral artery territory were studied in male Wistar rats that were either nonischemic control (n=34) or after exposure to transient middle cerebral artery occlusion (MCAO) by filament occlusion for 2 hours with 30 minutes of reperfusion (MCAO; n=38). The relationships among pressure-induced tone, smooth muscle calcium (using Fura 2), and membrane potential were determined. Sensitivity of the contractile apparatus to calcium was measured in permeabilized arterioles using Staphylococcus aureus α-toxin. Reactivity to inhibition of transient receptor potential melastanin receptor type 4 (9-phenanthrol), Rho kinase (Y27632), and protein kinase C (Gö6976) was also measured.
Results:
After MCAO, PAs had increased myogenic tone compared with controls (47±2% versus 35±2% at 40 mm Hg; P<0.01), without an increase in smooth muscle calcium (177±21 versus 201±16 nmol/L; P>0.05) or membrane depolarization (-38±4 versus -36±1 mV; P>0.05). In α-toxin-permeabilized vessels, MCAO caused increased sensitivity of the contractile apparatus to calcium. MCAO did not affect dilation to transient receptor potential melastanin receptor type 4 or protein kinase C inhibition but diminished dilation to Rho kinase inhibition.
Conclusions:
The increased vasoconstriction of PAs during early postischemic reperfusion seems to be due to calcium sensitization of smooth muscle and could contribute to infarct expansion and limit neuroprotective agents from reaching their target tissue.
Related Concept Videos
Vascular Spasm
Smooth Muscle Contraction
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
Autoregulation of Blood Flow
Chemical Signaling in Autoregulation
Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation....
Antihypertensive Drugs: Action of Calcium Channel Blockers
Ischemic Stroke ll: Pathophysiology
Nitric Oxide Signaling Pathway

