Oxygen and vascular smooth muscle contraction revisited

Abstract

The relationship between oxygen pressure measured in a tissue bath (PBO2) and the contractile tension produced by an agonist (contractile responsiveness) was studied in a series of experiments using helical strips cut from thoracic aortas, femoral and deep femoral arteries, and small arteries taken from red and white skeletal muscle of the rabbit. The wall thicknesses of these samples ranged from 200 micron for aortas down to approximately 20 micron for the smallest skeletal muscle arteries. Contractile responsiveness of all samples became progressively depressed when PBO2 was reduced stepwise. The depression produced in the large thick-walled samples occurred at higher PBO2 levels than that produced in the small thin-walled samples. Responsiveness of all of the artery samples was depressed by hypoxia more at low than at high levels of stimulation. In a second series of experiments PO2 at the surface of artery samples (PSO2) was measured using an oxygen-sensitive microelectrode. These measurements in conjunction with calculations of the PO2 within the arterial wall (PWO2) indicated that contractile responsiveness of both large and small artery samples became depressed when PWO2 fell below a lowest-value estimate of 50 Torr. From these findings it is concluded that 1) the sensitivity of vascular smooth muscle cells to hypoxia is similar for large and small arteries; 2) this sensitivity occurs in a range of PO2 that is physiologic for resistance vessels in situ; and 3) this sensitivity to hypoxia cannot be explained by an anoxic core hypothesis and may or may not involve restricted energy metabolism.

Developmental Changes in Thickness, Contractility, and Hypoxic Sensitivity of Newborn Lamb Cerebral Arteries

“…Although vessel thickness has been cited as a major determinant of the magnitude of relaxation (15), other factors clearly must be involved because the magnitudes of relaxation decreased in the common carotid , posterior communicating, and rostral choroidal arteries while vessel thicknesses were increasing with age. Because all responses to hypoxia were obtained under condit ions of complet e membrane depolarization , it is doubtful that differences in the effects of hypoxia on membrane hyperpolarization (16,17) could have contributed to the observed age-related differences in response to hypoxia. Similarly, it is doubtful that hypoxia-induced changes in sodiumcalcium exchange (18) were involved since extracellular sodium concentration during hypoxia was too low to support this mechanism (19).…”

An investigation of the actions of diltiazem on rat aorta exposed to acute hypoxia followed by re‐oxygenation

“…A reduction in the contractility of vascular muscle during exposure to hypoxia has been demonstrated both in vivo (Craigen & Jennett, 1981) and in vitro (Detar & Bohr, 1968;Hellstrand et al, 1977;Chang & Detar, 1980). In addition, a rapid recovery of the contractile response on return to normoxia has also been shown (Ebeigbe, 1982).…”

Oxygen-sensitive calcium channels in vascular smooth muscle and their possible role in hypoxic arterial relaxation.

“…Nevertheless, the mechanisms underlying this physiological response to low P02 remain largely unknown. Based on studies done in organ bath preparations, it is believed that oxygen influences vascular resistance by directly interfering with the rise of cytosolic Ca2+ required for contraction of smooth muscle cells (4)(5)(6)(7); nevertheless, very little is understood about oxygen-regulated processes in arterial myocytes. It has been suggested that dilatation of the coronary artery (8,9), and perhaps other arteries, in response to extreme hypoxia might be mediated by myocyte hyperpolarization in response to the opening of ATP-regulated K+ channels.…”