V o l . 181, N o . 1 , 1991 November 27, 1991 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS Pages 486-492 SUMMARY: Insulln has cardlovascular actlons and patlents wlth essentlal lypgrte-nglon dlsplay lnsulln reslstance. A cross-seCtlonal study of the RI RFLP of the lnsulln receptor gene (II\ISR) was carrled out ln 67 hypertenslve (HT) and 75 normotenslve (Nt) subjects whose parents had a slmilar blood pressure status at age >5O. The frequency of the mlnor (+) allele was O.3l ln HTs and O.44 ln NTs, and the difference between observed alleles ln all subjects in each group was slgnificant (72 = 4.8, P<O.O5).Nlele frequencles of a BgU. RFLP of the lnsulln gene, however, dld not dlffer between the HT and NT giroups. The data thus provlde evldence ln favour of an assoclatlon of H-T llth a polymorphlsm at the INS-Rloc-uq (19p13.3-13.2), so tmpltcattng thls locus, and posslbly a genetic varlant of the lnsulin receptor ltsef, in HT.- O 1991 Acadenic press, Inc. ASSOCIATION OF A RFLP FOR THE INSULIN RECEPTOR GENE, BUT NOT INSULIN, WITH ESSENTIAL IITPERTENSION Li-Hua Ying, Robert Y.L. Zee, Lyn R. Griffiths and Brian J. Morris* Molecular BiDlogA & Hgpertension La,boratory, Department oJ phg siologu, The"AniuerE itg oJ Sgdne a, N.S.w]b o ob, ers ti a Received October 14, 1991 Genotype is considered to be the primary underlying factor responsible for essential (primary; hypertension (HT), a disorder which affects -2Oo/o of the adult population [f ,2]. In the face of such a primary genetic 'defect', environmental factors, such as a diet high in NaCl, trigger a chronic rise in blood pressure [1,2]. To date the few molecular genetic studies that have been carried out using candidate gene probes have failed to demonstrate a significant association or linkage with HT [3-6]. Patients with HT often display insulin resistance and it has been suggested that this may play a role in the clinical course of the disease [Z-f f]. Under normal conditions lnsulin appears to have cardiovascular actions. These include stimulation of renal sodium reabsorption, vascular smooth muscle contraction and proliferation, and sympathetic activity [1o,11]. Moreover, such changes, elicited by mechanisms that are not yet completely understood, have also been implicated in the development of HT [12]. It was therefore o'f lnterest to examine whether genetic variants of the insulin receptor gene (INSR) and insulin gene (INS) co-segregate vrith HT. * To whom correspondence should be addressed. 0006-29txt9r $1.50 Copyright @ 1991 by Academic Press, Inc. AII rights of reproduction in any form reserved. 486