We have previously shown that the vasopressor effect of angiotensin II (Ang II) is inhibited by lipoxygenase (LO) blockers. To elucidate the specific mechanism involved, we studied the relationship between the contractile effect of Ang II and LO products in a human placental preparation. In perfused placental cotyledons, Ang II (boluses of 1 to 10 microg) increased perfusion pressure and 12-hydroxyeicosatetraenoic acid (12-HETE) release. The LO blockers phenidone and n-propyl gallate reduced the maximal Ang II-induced increment in pressure from 26+/-3 to 16+/-3 and 18+/-4 mm Hg, respectively (P<.05 for both). Ang II alone (10 microg) increased 12-HETE release from 8.9+/-3.6 to 37.6+/-0.4 ng/min, and this rise was entirely blocked by both phenidone and n-propyl gallate. Pressure increase generated by an increase in flow rate had no effect on 12-HETE formation. In deendothelialized umbilical artery segments, Ang II (10(-7) mol/L) increased 12-HETE formation by 47+/-5% (n=20). In cultured umbilical artery smooth muscle cells, Ang II increased 12-HETE formation from 48.1+/-7.2 to 75.1+/-15.3 ng/mg protein, and this effect was also blocked by the specific LO inhibitor baicalein (10(-6) mol/L). These results provide evidence that the vasopressor effect of Ang II is functionally coupled to 12-LO activation, which apparently takes place in arterial smooth muscle cells.

Hypertension is often cited as a risk factor for erectile dysfunction. To clarify the relation between hypertension and erectile dysfunction, we evaluated 32 consecutive hypertensive and 78 normotensive impotent men with respect to multiple potential determinants and parameters of erectile function, including medical and sexual history, depression, hormonal profile, penile nocturnal tumescence, penile vascular supply, and pudendal nerve conduction. The hypertensive men were older, had higher body mass index, and used more medications than the normotensive men. The groups were not different with respect to the prevalence of smoking and peripheral vascular disease, but the hypertensive men had a marginally higher rate of ischemic heart disease (P = .06). The prevalence of depression, abnormal nocturnal penile tumescence, anomalous pudendal nerve conduction, and impairment in arterial supply as determined by penile brachial index were similar in the two groups. Testosterone and bioavailable testosterone levels were lower in the hypertensive men. After stratification by age and body mass index, hypertensive men younger than 50 years with body mass index less than 30 kg/m2 had significantly lower testosterone levels (12.0 +/- 1.7 versus 21.3 +/- 1.4 nmol/L, P < .02) but not bioavailable testosterone levels (3.9 +/- 0.7 versus 6.4 +/- 0.7 nmol/L, P < .17) than the corresponding normotensive group. Prolactin, follicle-stimulating hormone, and luteinizing hormone levels of the two groups were not significantly different. Contrary to common belief and with the exception of lower circulating testosterone levels, the overall analysis showed little difference between hypertensive and normotensive men with respect to a wide range of classic determinants of erectile function. Direct study of the local vascular erectile apparatus appears necessary for further elucidation of the mechanisms underlying erectile dysfunction in hypertensive men.

We have previously reported that the nonselective lipoxygenase inhibitor phenidone is a potent hypotensive agent in the spontaneously hypertensive rat (SHR). In the present study, we examined the relationship between production of platelet 12-hydroxyeicosatetraenoic acid (12-HETE) and intra-arterial blood pressure in SHR and Wistar-Kyoto rats (WKY) using both a cross-sectional analysis and an acute pharmacological intervention. Basal generation rate of 12-HETE by platelets collected from the SHR was approximately 3.7-fold higher than in the WKY (0.86 +/- 0.24 versus 0.23 +/- 0.05 nmol/mL per 10 minutes, respectively; P < .01). Systolic arterial pressure was positively related to platelet 12-HETE formation rate when the entire rat population was considered (r = .70, P < .001). The specific 12-lipoxygenase inhibitor cinnamyl-3,4-dihydroxycyanocinnamate induced lowering of both arterial blood pressure and platelet 12-lipoxygenase activity in SHR. At 15 mg/kg, cinnamyl-3,4-dihydroxycyanocinnamate elicited a marked hypotensive effect in SHR but not in WKY. This reduction in arterial pressure was accompanied by an approximate 70% inhibition in platelet 12-HETE production rate. The return of high blood pressure to basal levels was associated with a significant rise in the production of platelet 12-HETE toward control values (baseline, 0.97 +/- 0.33 nmol/mL per 10 minutes; nadir of blood pressure, 0.19 +/- 0.03; resumption of basal pressure, 0.42 +/- 0.14). In contrast, captopril (15 mg/kg) induced a quantitatively similar decrease in blood pressure but had no effect on platelet 12-HETE generation rate. Thus, hypertension in SHR is linked to increased production rate of platelet 12-HETE. Acute blood pressure reduction attained during lipoxygenase inhibition but not by angiotensin converting enzyme inhibition leads to a concomitant reduction in the production of platelet 12-HETE. We speculate that since rat arterial tissue produces 12-HETE, increased 12-lipoxygenase activity in SHR may contribute to the maintenance of elevated arterial pressure in this strain.

We have observed seven initially obese individuals who, during the course of a strenuous weight-reduction program, developed diabetes mellitus: non-insulin-dependent diabetes mellitus in five cases and insulin-dependent diabetes mellitus in two cases. None had any sign of prior diabetic symptoms. Although weight reduction is encouraged in obesity, crash diets without proper medical surveillance may have deleterious effects. This sequence of induction of diabetes has not previously been reported in the medical literature. The metabolic situation in extremely low-calorie diets may be comparable to that in starvation. An attempt is made to explain our observation concerning the induction of a diabetic state during such diets, on the basis of increased insulin resistance in states of starvation and anorexia nervosa, with a concomitant role in stress hormones.

Diabetic MedicineVolume 12, Issue 3 p. 277-277 Severe Deterioration in Cognitive Function and Personality in Patients with Long-standing Diabetes E.S. Kisch, E.S. Kisch Department of Endocrinology, Ichilov Hospital, Tel-Aviv, IsraelSearch for more papers by this author E.S. Kisch, E.S. Kisch Department of Endocrinology, Ichilov Hospital, Tel-Aviv, IsraelSearch for more papers by this author First published: March 1995 https://doi.org/10.1111/j.1464-5491.1995.tb00473.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume12, Issue3March 1995Pages 277-277 RelatedInformation

International Journal of DermatologyVolume 31, Issue 5 p. 341-342 PACHYDERMOPERIOSTOSIS WITH NEW CLINICAL AND ENDOCRINOLOGIC MANIEESTATIONS SARAH BRENNER M.D., SARAH BRENNER M.D. Departments of Dermatology and Endocrinology, Tel Aviv Medical Center, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, IsraelSearch for more papers by this authorAVIGDOR SREBRNIK M.D., Corresponding Author AVIGDOR SREBRNIK M.D. Departments of Dermatology and Endocrinology, Tel Aviv Medical Center, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, IsraelAddress for correspondence: Avigdor Srebrnik, M.D., Department of Dermatology, Tel Aviv Medical Center, 6 Weizman Street, Tel Aviv 64239, Israel.Search for more papers by this authorELDAD S. KISCH, ELDAD S. KISCH Departments of Dermatology and Endocrinology, Tel Aviv Medical Center, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, IsraelSearch for more papers by this author SARAH BRENNER M.D., SARAH BRENNER M.D. Departments of Dermatology and Endocrinology, Tel Aviv Medical Center, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, IsraelSearch for more papers by this authorAVIGDOR SREBRNIK M.D., Corresponding Author AVIGDOR SREBRNIK M.D. Departments of Dermatology and Endocrinology, Tel Aviv Medical Center, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, IsraelAddress for correspondence: Avigdor Srebrnik, M.D., Department of Dermatology, Tel Aviv Medical Center, 6 Weizman Street, Tel Aviv 64239, Israel.Search for more papers by this authorELDAD S. KISCH, ELDAD S. KISCH Departments of Dermatology and Endocrinology, Tel Aviv Medical Center, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, IsraelSearch for more papers by this author First published: May 1992 https://doi.org/10.1111/j.1365-4362.1992.tb03951.xCitations: 5AboutRelatedInformationPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessClose modalShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume31, Issue5May 1992Pages 341-342 RelatedInformation RecommendedClinical and physiological heterogeneity in slow transit constipation: a review of 122 patients Knowles, Scott, Williams, Lunniss, Colorectal DiseasePatient perceptions of factors leading to spasmodic dysphonia: A combined clinical experience of 350 patientsLesley Childs MD, Scott Rickert MD, Thomas Murry PhD, Andrew Blitzer MD, DDS, Lucian Sulica MD, The LaryngoscopeMolecular and clinical overlap of Angelman and Prader‐Willi syndrome phenotypesA. J. Kirkilionis, A. E. Chudley, C. A. Gregory, J. L. Hamerton, American Journal of Medical GeneticsNew polymer‐chemical developments in clinical dental polymer materials: Enamel–dentin adhesives and restorative compositesNorbert Moszner, Thomas Hirt, Journal of Polymer Science Part A: Polymer ChemistryAssociation between comorbidity and clinical characteristics of MSR. A. Marrie, R. I. Horwitz, G. Cutter, T. Tyry, T. Vollmer, Acta Neurologica Scandinavica

Letters and Corrections15 August 1988Nonsteroidal Anti-Inflammatory Drugs, and HypertensionEldad S. Kisch, MD, PhD, Benno Fischel, MD, Michael Yaron, MDEldad S. Kisch, MD, PhDSearch for more papers by this author, Benno Fischel, MDSearch for more papers by this author, Michael Yaron, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-109-4-344_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor: That the effect of nonsteroidal anti-inflammatory drugs on blood pressure remains a concern is reflected in the recent article by Radick and colleagues (1). We believe that the conflicting reports on this issue are probably due to nonhomogeneity of populations studied for plasma renin status.In 1977 we presented data at the annual scientific meeting of the Israel Endocrine Society, showing that in two groups of patients, one with labile or borderline hypertension and the other with rheumatoid arthritis, blood pressure rose after administration of indomethacin therapy only in some patients who had initial low plasma renin...References1. RadackDeckBloomfield KCS. Ibuprofen interferes with the efficacy of antihypertensive drugs: a randomized, double-blind, place-bo-controlled trial of Ibuprofen compared with acetaminophen. Ann Intern Med. 1987;107:628-35. LinkGoogle Scholar2. Gerber J. Indomethacin-induced rises in blood pressure. Ann Intern Med. 1983;99:555-8. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Ichilov Hospital Tel-Aviv, 64239, Israel PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 August 1988Volume 109, Issue 4Page: 344-344KeywordsBlood plasmaBlood pressureDrugsEndocrine therapyHypertensionPopulation statisticsRheumatoid arthritis Issue Published: 15 August 1988 PDF DownloadLoading ...

Insulin-treated diabetics were questioned about stressful events preceding the onset of their diabetes, such as: 1) febrile disease, 2) accident, 3) pregnancy, 4) problems in the family or at work, 5) other or 6) no specific events. Of 66 patients there were 38 men and 28 women, with ages ranging from 17 to 85 years. The duration of diabetes was from several months to 30 years; 41% had no family history of diabetes. Forty-nine patients (74%) indicated a specific event (mostly groups 4 and 5), preceding the onset of diabetes by several months in 24, weeks in 11, and days in 10 patients; 4 did not remember a time sequence. Only 31% of a control group of 62 age- and sex-matched acute surgical patients, similarly questioned, indicated a specific event prior to their operation. Although these data were not intended to prove a cause-and-effect relationship, they suggest some connection between stressful events and disruption of metabolic equilibrium in persons susceptible (genetically or otherwise) to developing diabetes mellitus.