Abstract
Several studies suggest that DHEAS is a protective factor against atherosclerosis and coronary artery disease in man, but the mechanism of its biological role is unclear. Recently, it has been suggested that DHEAS can retard atherosclerosis formation through an increase in nitric oxide (NO) production by increasing E2 synthesis. The aim of the study was to evaluate the platelet cGMP concentrations (i.e. a marker of NO production) and the serum levels of DHEAS and E2 in normal females. Blood samples were taken from 51 normal women (age 42.3±1.9 yr, range: 22–67 yr, BMI 23.0±0.6 kg/m2) to evaluate platelet cGMP concentrations and serum levels of DHEAS and E2. To determine the platelet cGMP content, platelet rich plasma (PRP) was incubated at 37 C (30 min) in the presence of IBMX. The amount of platelet cGMP was measured by a cGMP (3H) assay kit. In all subjects the mean of platelet cGMP was 536.2±45.3 fmol/106 platelets and the mean of serum DHEAS and E2 was 151.4±13.9 μg/dl and 34.7±6.1 pg/ml, respectively. In all subjects DHEAS positively correlates with cGMP (p<0.001, r=0.513) and with E2 (p<0.001, r=0.650); furthermore E2 positively correlates with cGMP (p<0.001, r=0.663). In conclusion our data support the hypothesis that DHEAS exerts its antiatherogenic effect by increasing the NO production directly and/or by increasing the E2 synthesis.
Similar content being viewed by others
References
Orentreich N., Brind J.L., Rizer R.L., Vogelman J.H. Age changes and sex differences in serum dehydroepiandrosterone sulfate concentrations throughout adulthood. J. Clin. Endocrinol. Metab. 1984, 59: 551–555.
Thomas G., Frenoy N., Legrain S., Sebag-Lanoe R., Baulieu E.E., Debuire B. Serum dehydroepiandrosterone sulfate levels as an individual marker. J. Clin. Endocrinol. Metab. 1994, 79: 1273–1276.
Vermeulen A. Dehydroepiandrosterone sulfate and aging. Ann. NY Acad. Sci. 1995, 774: 121–127.
Hobbkirk R. Steroid sulfotransferases and steroid sulfate sulfatases: characteristics and biological roles. Can. J. Biochem. Cell. Biol. 1985, 63: 1127–1144.
Rao L.G.S. Urinary steroid-excretion patterns after acute myocardial infarction. Lancet 1970, 22: 390–391.
Barret-Connor E., Khaw K.T., Yen S.S. A prospective study of dehydroepiandrosterone sulfate, mortality and cardiovascular disease. N. Engl. J. Med. 1986, 315: 1519–1524.
Yasushi M., Hirofumi Y., Michihiro Y., Yuji M., Koichi N., Ryusuke T., Hiroaki K., Kiyotaka K., Hisao O., Yoshihiko S., Kasuwa N. The plasma levels of dehydroepiandrosterone sulfate are decreased in patients with chronic heart failure in proportion to the severity. J. Clin. Endocrinol. Metab. 2000, 85: 1834–1840.
Nestler J.E., Barlascini C.O., Clore J.N., Blachard W.G. Dehydro-epiandrosterone reduces serum low density lipoprotein level and body fat but does not alter insulin sensitivity in normal man. J. Clin. Endocrinol. Metab. 1988, 66: 57–61.
Gordon G.B., Bush D.E., Weisman H.F. Reduction of atherosclerosis by administration of dehydroepiandrosterone. A study in the hypercholesterolemic New Zealand white rabbit with aortic intimal injury. J. Clin. Invest. 1988, 82: 712–720.
Eich D.M., Nestler J.E., Johnson D.E., Dworkin G.H., Daijin K., Wechsler A.M., Hess M.L. Inhibition of accelerated coronary atherosclerosis with dehydroepiandrosterone in the heterotopic rabbit model of cardiac transplantation. Circulation 1993, 87: 261–269.
Dworkin C.R., Gorman S.D., Pashko L.L., Christofalo V.J., Schwartz A.G. Inhibition of growth of HeLa and WI-38 cells by dehydroepiandrosterone and its reversal by ribo and deoxiri-bonucleosides. Life Sci. 1986, 38: 1451–1457.
Jesse R., Nestler J., Eich D., Hess M. Dehydroepiandrosterone in vivo and in vitro inhibits platelet aggregation. J. Am. Coll. Cardiol. 1991, 17 (Suppl. A): 376 A.
Hayashi T., Esaki T., Muto E., Kano H., Asai Y., Thakur N.K., Sumi D., Jayachandran M., Iguchi A. Dehydroepiandrosterone retards atherosclerosis formation through its conversion to estrogen. The possible role of nitric oxide. Arterioscler. Thromb. Vasc. Biol. 2000, 20: 782–792.
Schray-Utz B., Zeiher A.M., Busse R. Expression of constitutive NO synthase in cultured endothelial cells is enhanced by 17β-estradiol. Circulation 1993, 88: I80 (Abstract 0416).
Niu X.F., Smith C.W., Kubes P. Intracellular oxidative stress induced by nitric oxide synthesis inhibition increases endothelial cell adhesion to neutrophils. Circ. Res. 1994, 74: 1133–1140.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Martina, V., Origlia, C., Bruno, G.A. et al. Serum DHEAS levels correlate with platelet cGMP in normal women. J Endocrinol Invest 24, 28–30 (2001). https://doi.org/10.1007/BF03343922
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/BF03343922