Gender Differences In Vascular Reactivity Research Articles

Gender differences in vascular reactivity of mesenteric arterioles in portal hypertensive and non-portal hypertensive rats.

BACKGROUNDPortal hypertension (PHT) is primarily caused by an increase in resistance to portal outflow and secondarily by an increase in splanchnic blood flow. Vascular hyporeactivity both in systemic circulation and in the mesenteric artery plays a role in the hyperdynamic circulatory syndrome.AIMTo explore gender differences and the role of endogenous sex hormones in PHT and vascular reactivity of mesenteric arterioles in rats.METHODSCirrhosis and PHT were established by subcutaneous injection of carbon tetrachloride (CCl4) in both male and female integral and castrated rats (ovariectomized [OVX] in female rats, orchiectomy [ORX] in male rats). The third-order branch of the mensenteric artery was divided and used to measure vascular reactivity to vasoconstrictors.RESULTSNo significant difference in portal pressure was observed between integral and castrated male PHT rats (15.2 ± 2.1 mmHg vs 16.7 ± 2.7 mmHg, P > 0.05). The portal pressure in integral female PHT rats was lower than that in OVX female PHT rats (12.7 ± 2.7 mmHg vs 16.5 ± 2.4 mmHg, P < 0.05). In PHT rats, the concentration response curves of the mesenteric arterioles to norepinephrine were shifted to the right, and the maximal responses (Emax) values were decreased and effective concentrations causing half maximum responses (EC50) values were increased, compared to those of non-PHT rats, both in male and female rats. Compared to non-PHT integral male rats, the sensitivity of the mesenteric arterioles of non-PHT ORX male rats to norepinephrine was decreased (P > 0.05). However, there was no difference between integral and ORX male rats with PHT. In integral female PHT rats, the concentration response curves were shifted to the left (P < 0.05), and the Emax values were increased and EC50 values were decreased compared to OVX female PHT rats.CONCLUSIONClear gender differences were observed in mesenteric vascular reactivity in CCl4-induced cirrhotic and PHT rats. Conservation of estrogen can retain the sensitivity of the mesenteric arterioles to vasoconstrictors and has a protective effect on splanchnic vascular function in PHT.

Gender Differences in Vascular Reactivity of Aortas from Streptozotocin-Induced Diabetic Mice

The aim of the present study was to assess gender differences in diabetes-related vascular reactivity in murine aortas. Diabetes is a risk factor for ischemic heart disease, cerebral ischemia, and atherosclerosis, conditions in which endothelial dysfunction plays a pathogenetic role. We examined vascular responses in aortas isolated from streptozotocin (STZ)-induced type 1 diabetic mice and age-matched control mice, and looked for gender differences in the diabetes-induced changes in these responses. For each gender, the plasma adiponectin levels were lower in diabetic mice than in the controls, and they were significantly higher in females than in males. The acetylcholine (ACh)-induced endothelium-dependent relaxation of aortic rings was impaired (vs. that in the age-matched controls) in diabetic male mice, but not in diabetic female mice. The sodium nitroprusside-induced endothelium-independent aortic relaxation was not altered by diabetes in either male or female mice. The norepinephrine-induced aortic contraction was enhanced (vs. that in the control group) in diabetic female mice, but not in diabetic male mice, whereas in the presence of N(G)-nitro-L-arginine neither gender exhibited a significant diabetes-induced change in this contraction. The clonidine-induced and insulin-induced endothelium-dependent aortic relaxations were impaired only in the diabetic female group (vs. the age-matched controls). These results suggest that: a) in male diabetic mice, which exhibited low adiponectin levels, these were impairments of both the aortic relaxation and nitric oxide (NO) production induced by ACh, whereas b) in female diabetic mice, there were impairments of the aortic relaxations induced by both insulin and clonidine.

Gender differences in vascular reactivity to endothelin-1 (1-31) in mesenteric arteries from diabetic mice

Endothelin-1 (1-31) [ET-1 (1-31)], a novel member of the ET family, comprises 31 amino acids and is derived from the selective hydrolysis of big ET-1 by chymase. Although ET-1 (1-31) reportedly exerts biological effects by direct or indirect [via its conversion to ET-1 (1-21)] mechanisms, it is unclear whether in diabetes the vascular effects of ET-1 (1-31) display gender differences. We investigated this question by exposing mesenteric artery rings to ET-1 (1-31), using arteries from mice in the early or chronic phase of diabetes. In the early stage of diabetes, the ET-1 (1-31)-induced contraction was similar between age- and sex-matched control and streptozotocin (STZ)-induced diabetic mice. In the chronic stage of diabetes, the ET-1 (1-31)-induced contraction was enhanced in diabetic female mice, but not in diabetic male mice (vs. both age-matched control and early-stage diabetic mice). This enhancement was largely prevented by Y27632 (Rho kinase inhibitor), PD98059 [inhibitor of extracellular signal related kinases 1 and 2 (ERK1/2)], or SP600125 [C-jun terminal kinase (JNK) inhibitor]. These data indicate that the ET-1 (1-31)-induced vasoconstriction in the mesenteric artery may be specifically enhanced in established diabetic female mice, and that this enhancement may be due to alterations in the activities of Rho/Rho kinase or mitogen-activated protein kinase.

Gender differences in vascular reactivity of aortas from rats with and without portal hypertension

Inflammatory responses related to portal hypertension may be different in male and female rats. Most experimental studies of portal hypertension have involved male animals, and little information is available on gender differences in this setting. The aim of the present study was to compare aortic reactivity in female and male rats with and without portal hypertension. Contraction response curves to phenylephrine were studied with aortic rings, with and without endothelium. For relaxation studies, rings were precontracted with phenylephrine 10(-7) mol/L and then exposed to acetylcholine 10(-4) mol/L. Portal hypertension was provoked by calibrated portal stenosis performed 2 weeks before experiments. In non-hypertensive conditions, the contractile response to increasing phenylephrine concentrations was significantly stronger in rings from male than female rats, both with and without endothelium. In male rats with portal hypertension, the phenylephrine concentration-response curves were lowered and shifted to the right in aortic rings both with and without endothelium. In female rats, portal hypertension did not induce significant changes in the phenylephrine concentration-response curves. In female rats, portal hypertension induced a marked increase in relaxation (157 +/- 123% vs 81 +/- 64% in controls); the increase was also stronger than that in male rats with portal hypertension (95 +/- 6%; P < 0.01). Clear gender differences were observed in vasoconstrictor responsiveness of aortic rings from rats with and without portal hypertension. Contrary that in male rats, portal hypertension did not induce vascular hyporesponsiveness in female rats. Further investigations are required to explain these differences.

Gender differences in vascular reactivity to levosimendan in rat aortic rings

Gender differences in vascular reactivity to levosimendan in rat aortic rings

Gender Differences in Cardiovascular Responses to Sphygmomanometric Measurements

Objective: To study gender differences of cardiovascular responses due to painful stimuli during sphygmomanometry. Methods: We studied 80 subjects (40 women, 40 men). Blood pressure (BP) was determined continuously and noninvasively using a Finapres device (Penaz technique). The painful stimulus was administered by inflating the arm cuff of a sphygmomanometric device to 300 mmHg maximum pressure. Results: During cuff inflation systolic blood pressure (SBP) increased in women (+3.7 mmHg, SD = 9.9), but was unchanged in men (repeated measures ANOVA, P &lt; .05). Diastolic blood pressure (DBP) and heart rate did not show significant changes. Cycle and oral contraceptives did not influence cardiovascular reactivity in the female subpopulation. Women reported a different pain quality but not intensity. Conclusions: Women and men exhibit a slightly different vascular reactivity to painful stimuli. Since cycle and hormonal contraception did not influence reactivity, hormonal influences seem to play a minor role. However, different pain perception might account for gender differences in vascular reactivity.

Gender differences in vascular reactivity to endothelin-1 in deoxycorticosterone-salt hypertensive rats.

In experimental models of hypertension, blood pressure reaches a higher level in male than in female rats. Because endothelin-1 (ET-1) seems to play a role in blood pressure elevation in deoxycorticosterone acetate (DOCA)-salt hypertension, we hypothesized that male DOCA-salt rats would display a greater vascular responsiveness to ET-1 than female DOCA-salt rats. Male and female Wistar rats were uninephrectomized, received DOCA injections (50 mg/kg/week) and water plus 1.0% NaCl/0.2% KCl. Control rats received vehicle and tap water. Responses to ET-1, norepinephrine (NE), serotonin (5-HT), IRL-1620, a selective endothelin-B- (ET(B)) receptor agonist, and acetylcholine (ACh) were evaluated in isolated aortic rings and also in vivo in the mesenteric microcirculation. Endothelium-intact aortas from male and female DOCA rats displayed increased sensitivity (p < 0.05) to NE and 5-HT, but decreased relaxation to ACh in comparison to aortas from respective control male and female rats. Endothelium-denuded, but not endothelium-intact, arteries from male DOCA rats displayed increased sensitivity (-log EC20) to ET-1, but no changes in ET-1 sensitivity were observed in female DOCA aortas. IRL-1620 induced contraction in male DOCA aortas, but not in female DOCA or control endothelium-denuded aortas. In the microcirculation, IRL-1620 induced vasodilation in male and female control rats, but marked vasoconstriction in male DOCA and minimal changes in vessels diameter in female DOCA rats. Bosentan, an ET(A)/ET(B)-receptor antagonist, induced a greater decrease in mean arterial blood pressure in male than in female DOCA-salt hypertensive rats. These data support the hypothesis that DOCA-salt rats exhibit gender differences in ET-1 vascular reactivity, which probably result from functional changes in ET(B)-receptors. The increased ET(B) responses in male DOCA-salt hypertensive rats may play a role in their higher blood pressure levels.

Gender Differences in Vascular Reactivity to Endothelin-1 in Deoxycorticosterone-Salt Hypertensive Rats

Gender Differences in Vascular Reactivity to Endothelin-1 in Deoxycorticosterone-Salt Hypertensive Rats

Gender differences in vascular reactivity in hamsters fed a cholesterol diet

Gender differences in vascular reactivity in hamsters fed a cholesterol diet