Long-term Effects of UV Light on Contractility of Rat Arteries In Vivo¶
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Several studies have shown that UV irradiation may be effective for preventing vascular restenosis or vasopasm. However, the long-term effects of UV light on the physiological properties of vessels such as arterial tension have not been elucidated. We therefore studied the long-term effects of UV using rat carotid arteries treated with UV-B light (wavelength = 313 nm, total energy = 14 mJ/mm2). The animals were sacrificed at 1, 7 and 14 days after UV light exposure, and the carotid arteries were studied by light microscopy and the contractile responses of isolated arterial rings were recorded under isometric tension. UV treatment had induced a substantial loss of smooth muscle cells (SMC) along the entire circumference of the media on days 7 and 14, whereas loss of SMC on day 1 was negligible. Contractile responses of arteries that had been exposed to UV light were significantly reduced on days, 1, 7 and 14. The susceptibility of UV-treated arteries to phenylephrine and prostaglandin F2 alpha was significantly decreased on days 1 and 7, but decreased susceptibility was not seen on day 14. Acetylcholine-induced relaxations were not altered by UV treatment. These results suggest that the long-term effect of UV light is an attenuation of smooth muscle contractility without impairment of endothelial function.Keywords:
Contractility
Phenylephrine
Mesenteric arteries
Coronary arteries
Phenylephrine pivalate has been assumed to be a prodrug devoid of important intrinsic activity because of its structural similarity to dipivefrin (dipivaly epinephrine). However, unlike dipivefrin, the pharmacologic activity of phenylephrine pivalate was not prevented by prior administration of echothiophate iodide. Rabbits pretreated bilaterally with 0.25% echothiophate for two and seven days had similar mydriasis, both in quantity and duration, after receiving 10% phenylephrine hydrochloride to one eye and 1% phenylephrine pivalate to the other eye. This as consistent with the hypothesis that the phenylephrine pivalate molecule has important alpha-adrenergic activity regardless of whether it is converted to phenylephrine.
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Abstract The purpose of these studies was to compare changes in conduit and resistance artery function in deoxycorticosterone-salt hypertensive rats. We hypothesized that if there was a common mechanism producing changes in vascular function in hypertension, then there would be similar alterations in reactivity of conduit and resistance arteries. Helically cut strips of common carotid artery were prepared for measurement of isometric force generation, and segments of small mesenteric arteries were pressurized for video dimension analysis. Sensitivity of arteries to phenylephrine and acetylcholine was determined. Carotid arteries from deoxycorticosterone-salt hypertensive rats were more sensitive to phenylephrine than arteries from control rats, whereas mesenteric resistance arteries from hypertensive rats were less sensitive to phenylephrine. In carotid arteries, endothelial denudation or incubation with N ω -nitro- l -arginine increased phenylephrine sensitivity in control rats to the level seen in deoxycorticosterone-salt rats. These manipulations had no effect on phenylephrine sensitivity in arteries from deoxycorticosterone-salt rats. In mesenteric resistance arteries, endothelium denudation normalized the depressed phenylephrine sensitivity in arteries from hypertensive rats but had no effect on arteries from normotensive rats. This depressed phenylephrine sensitivity in deoxycorticosterone-salt mesenteric arteries was not reversed by incubation with N ω -nitro- l -arginine. Acetylcholine-induced relaxation was depressed in carotid arteries from deoxycorticosterone-salt hypertensive rats, and N ω -nitro- l -arginine blocked these relaxations. In contrast, acetylcholine relaxation in the mesenteric arteries from normotensive and hypertensive rats did not differ. N ω -nitro- l -arginine slightly but significantly attenuated acetylcholine dilation only in mesenteric resistance arteries from the hypertensive rats. We conclude that qualitatively different changes in vasoconstrictor sensitivity to phenylephrine occur in carotid arteries and mesenteric resistance arteries of deoxycorticosterone-salt hypertensive rats. The increased phenylephrine sensitivity in carotid arteries in this model of hypertension is due to the loss of endothelium-derived nitric oxide production. In contrast, the decreased phenylephrine sensitivity in mesenteric resistance arteries from deoxycorticosterone-salt rats is due to a non–nitric oxide–mediated influence of the endothelium that is absent in arteries from normotensive rats.
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Pupil dilation from commercially available phenylephrine compounds was studied in a group of 11 subjects. Phenylephrine 10% (aq) did not produce significantly more mydriasis than phenylephrine 2.5% (aq) in the general population (P less than 0.05). This suggests that phenylephrine 2.5% can be used instead of phenylephrine 10% for diagnostic dilation.
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Isolated human, Japanese monkey and dog epicardial coronary arteries and dog renal and mesenteric arteries treated with phentolamine responded to isoproterenol with a concentration-related relaxation. The KB values of metoprolol, a beta-1 antagonist, in the coronary arteries from different mammals did not differ, but were appreciably smaller than those in the dog renal and mesenteric arteries. Treatment with butoxamine, a beta-2 antagonist, inhibited the relaxation of dog mesenteric arteries to a greater extent than that of monkey and dog coronary arteries. Terbutaline, a beta-2 agonist, produced a greater relaxation in monkey mesenteric and dog renal and mesenteric arteries than in human, monkey and dog coronary arteries. Norepinephrine relaxed the monkey and dog coronary arteries dose-dependently via mainly beta-1 adrenoceptors, but elicited a contraction or a minute relaxation in dog mesenteric arteries even when treated with high concentrations of phentolamine. Contractile responses to electrical stimulation of adrenergic nerves in monkey coronary arteries were potentiated by treatment with metoprolol and propranolol, whereas the contractions in dog mesenteric arteries were unaffected. It is concluded that the amine-induced relaxation of human and monkey epicardial coronary arteries is mediated mainly by beta-1 adrenoceptor subtype, as is the response of dog coronary arteries. Involvement of beta-1 subtype in coronary artery relaxations would be a mechanism underlying potentiation by beta antagonists of the contraction caused by norepinephrine released from adrenergic nerves in primates.
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Objective To assess the alterations of morphological and functional properties of conductance coronary and mesenteric resistance arteries in spontaneously hypertensive rats (SHR). Design The in-vitro intrinsic elastic properties of the wall material in SHR coronary arteries were determined in comparison with those of Wistar–Kyoto (WKY) rats. Mesenteric resistance arteries from rats of both strains were also studied. Methods Arterial segments were cannulated at both ends using an arteriograph system and subjected to pressure increments with simultaneous measurements of the wall thickness and internal diameter. The strain, stress and incremental elastic modulus (Einc) were calculated from diameter–pressure curves. Results Over the full range of pressures tested (10–160 mmHg), the internal diameters of SHR coronary arteries were not significantly different from those of WKY rat arteries, whereas we observed that SHR mesenteric resistance arteries had a significantly smaller diameter. The stress-strain curve for coronary arteries was shifted significantly to the left-hand side for the SHR group indicating more stress per unit strain, whereas the opposite was found for mesenteric resistance arteries. When Einc was determined under isobaric conditions, we found no difference between SHR and WKY rat coronary arteries, whereas this parameter was decreased significantly for SHR mesenteric resistance arteries. When Einc was estimated at the respective operating pressures, it was 1.7- to 2.8-fold greater for SHR than it was for WKY rat mesenteric resistance and coronary arteries. Moreover, the total collagen area: lumen area ratio was significantly greater for the SHR than it was for the WKY rat coronary artery wall, but this ratio was similar for mesenteric preparations from the two strains. Conclusion These results show that, at a given stress or operating pressure level, the material of SHR coronary artery wall is characterized by an increase in Einc, whereas there is no increase in Einc for in mesenteric resistance arteries. This functional alteration is accompanied by an increase in the relative proportion of collagen, a component with a high elastic modulus, in the wall. In contrast, we found no change in elastic modulus and in the relative proportion of collagen for the SHR mesenteric resistance arteries. Furthermore, the present results support the hypothesis that alterations in distensibility differ among the components of the SHR vasculature.
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Mesenteric arteries
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Both phenylephrine and noradrenaline increased the force of contraction of isolated preparations of rabbit and chicken heart. Noradrenaline increased the rate of formation of cyclic 3′,5′-AMP in homogenate of rabbit or chicken heart, but phenylephrine did not. These results demonstrate that sympathomimetic amines can increase cardiac contractility without increasing the activity of adenyl cyclase.
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. Phenylephrine produced relaxation of the isolated guinea‐pig tracheal chain preparation, its potency being 1/5 that of noradrenaline on normal tissues. . The potentiation of phenylephrine by cocaine (10 −5 M) was only slight. Thus on cocaine‐treated tissues phenylephrine was 1/45 as potent as noradrenaline. . The dose‐response lines to phenylephrine were shifted in a parallel manner by propranolol 10 −8 M and 10 −7 M, suggesting that the relaxations were mediated through β‐adrenoceptors. . Phenylephrine had a lower intrinsic activity than the catecholamines and produced multiphasic dose‐response lines at the higher doses used in the presence of propranolol (10 −6 M). These observations have been explained by the evidence obtained that phenylephrine is a partial agonist with β‐adrenoceptor blocking activity. . From experiments using α‐adrenoceptor blocking drugs, it has been concluded that stimulation of α‐adrenoceptors has little influence on the β‐adrenoceptor relaxation to phenylephrine on the guinea‐pig tracheal chain preparation.
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