20
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Acute nitric oxide synthase inhibition induces greater increases in blood pressure in female versus male Wistar Kyoto rats

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Nitric oxide (NO) contributes to blood pressure (BP) regulation via its vasodilatory and anti‐inflammatory properties. We and others previously reported sex differences in BP in normotensive and hypertensive rat models where females have lower BP than age‐matched males. As females are known to have greater NO bioavailability than age‐matched males, the current study was designed to test the hypothesis that anesthetized female normotensive Wistar Kyoto rats (WKY) are more responsive to acute NOS inhibition‐induced increases in BP compared to male WKY. Twelve‐week‐old male and female WKY were randomized to infusion of the nonspecific NOS inhibitor N G‐nitro‐L‐arginine methyl ester (L‐NAME, 1 mg/kg/min) or selective NOS1 inhibition with vinyl‐L‐NIO (VNIO, 0.5 mg/kg/min) for 60 min. Mean arterial BP, glomerular filtration rate (GFR), urine volume, and electrolyte excretion were assessed before, and during L‐NAME or VNIO infusion. L‐NAME and VNIO significantly increased BP in both sexes; however, the increase in BP with L‐NAME infusion was greater in females versus males compared to baseline BP values. Acute infusion of neither L‐NAME nor VNIO for 60 min altered GFR in either sex. However, urine volume, sodium, chloride and potassium excretion levels increased comparably in male and female WKY with L‐NAME and VNIO infusion. Our findings suggest sex differences in BP responses to acute non‐isoform‐specific NOS inhibition in WKY, with females being more responsive to L‐NAME‐induced elevations in BP relative to male WKY. However, sex differences in the BP response did not coincide with sex differences in renal hemodynamic responses to acute NOS inhibition.

          Related collections

          Most cited references43

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Sex differences in primary hypertension

          Men have higher blood pressure than women through much of life regardless of race and ethnicity. This is a robust and highly conserved sex difference that it is also observed across species including dogs, rats, mice and chickens and it is found in induced, genetic and transgenic animal models of hypertension. Not only do the differences between the ovarian and testicular hormonal milieu contribute to this sexual dimorphism in blood pressure, the sex chromosomes also play a role in and of themselves. This review primarily focuses on epidemiological studies of blood pressure in men and women and experimental models of hypertension in both sexes. Gaps in current knowledge regarding what underlie male-female differences in blood pressure control are discussed. Elucidating the mechanisms underlying sex differences in hypertension may lead to the development of anti-hypertensives tailored to one's sex and ultimately to improved therapeutic strategies for treating this disease and preventing its devastating consequences.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Greater oxidative stress in healthy young men compared with premenopausal women.

            Coronary risk factors, including age, hypertension, diabetes mellitus, hyperlipidemia, and smoking, are associated with enhanced oxidative stress, which is implicated as a potential mechanism for atherogenesis and atherosclerotic cardiovascular diseases. Male sex is one of the well-known cardiovascular risk factors. We tested the hypothesis that oxidative stress is greater in men than in women. Plasma thiobarbituric acid-reactive substances (TBARS) and urinary 8-isoprostaglandin F2alpha (8-iso-PGF2alpha) were measured in 52 young men and 51 age-matched women. The subjects were healthy, were not smokers, and were not taking any medications or vitamins. Age, blood pressure, plasma cholesterol, and glucose did not differ between the groups. Baseline TBARS (2.32 +/- 0.11 [men] versus 1.87 +/- 0.09 [women] nmol/mL, P<0.01) and 8-iso-PGF2alpha (292 +/- 56 [men] versus 164 +/- 25 [women] pg/mg creatinine, P<0.05) were higher in men than in women. Supplementation of antioxidant vitamins for 4 weeks in men produced a significant reduction in TBARS and 8-iso-PGF2alpha by 34% (P<0.01) and 48% (P<0.05), respectively. Plasma superoxide dismutase, catalase, and vitamin E levels were comparable between the groups. Enhanced oxidative stress in men may provide a biochemical link between male sex and atherosclerotic diseases related to oxidative stress.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Mechanisms and consequences of endothelial nitric oxide synthase dysfunction in hypertension.

              Reduced nitric oxide bioavailability contributes to endothelial dysfunction and hypertension. The endothelial isoform of nitric oxide synthase (eNOS) is responsible for the production of nitric oxide within the endothelium. Loss of eNOS cofactor tetrahydrobiopterin to initial increase in oxidative stress leads to uncoupling of eNOS, in which the enzyme produces superoxide anion rather than nitric oxide, further substantiating oxidative stress to induce vascular pathogenesis. The current review focuses on recent advances on the molecular mechanisms and consequences of eNOS dysfunction in hypertension, and potential novel therapeutic strategies restoring eNOS function to treat hypertension.
                Bookmark

                Author and article information

                Contributors
                aelmarakby@augusta.edu
                Journal
                Physiol Rep
                Physiol Rep
                10.1002/(ISSN)2051-817X
                PHY2
                physreports
                Physiological Reports
                John Wiley and Sons Inc. (Hoboken )
                2051-817X
                07 August 2023
                August 2023
                : 11
                : 15 ( doiID: 10.1002/phy2.v11.15 )
                : e15771
                Affiliations
                [ 1 ] Departments of Oral Biology & Diagnostic Sciences Augusta University Augusta Georgia USA
                [ 2 ] Department of Pharmacology and Toxicology, Faculty of Pharmacy Mansoura University Mansoura Egypt
                [ 3 ] Departments of Physiology Augusta University Augusta Georgia USA
                Author notes
                [*] [* ] Correspondence

                Ahmed A. Elmarakby, Departments of Oral Biology & Diagnostic Sciences, Augusta University, 1459 Laney Walker Blvd, Augusta, GA 30912, USA.

                Email: aelmarakby@ 123456augusta.edu

                Author information
                https://orcid.org/0000-0002-3065-4457
                https://orcid.org/0000-0003-2649-9850
                Article
                PHY215771 PHYSREP-2023-04-096
                10.14814/phy2.15771
                10406564
                0479d983-3468-4b4f-af23-fda4fd6382f2
                © 2023 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 29 June 2023
                : 27 April 2023
                : 02 July 2023
                Page count
                Figures: 3, Tables: 2, Pages: 9, Words: 5815
                Funding
                Funded by: American Heart Association (AHA)
                Award ID: 17EIA33410565
                Funded by: HHS | National Institutes of Health (NIH) , doi 10.13039/100000002;
                Award ID: HL‐12709
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                August 2023
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.3.2 mode:remove_FC converted:07.08.2023

                blood pressure,l‐name,renal hemodynamics,sex,vnio,wky
                blood pressure, l‐name, renal hemodynamics, sex, vnio, wky

                Comments

                Comment on this article