title: Estrogen therapy may counterbalance eutrophic remodeling of coronary arteries and increase bradykinin relaxation in a rat model of menopausal hypertension.
abstract: Hypertension causes adverse remodeling and vasomotor alterations in coronaries. Hormones such as estrogen may help counterbalance some of these effects. The aim of this study was to analyze the effects of ovariectomy and estrogen therapy in a rat model of menopausal hypertension induced by angiotensin II (AII).
  
  
  
  We investigated diameter, tone, and mechanics of intramural coronaries taken from ovariectomized female rats (n = 11) that received chronic AII treatment to induce hypertension, and compared the results with those found in female rats that were also given estrogen therapy (n = 11). The "hypertensive control" group (n = 11) underwent an abdominal sham operation, and received AII. After 4 weeks of AII treatment, side branches of left anterior descendent coronary (approximately 200 μm in diameter) were isolated, cannulated with plastic microcannulas at both ends, and studied in vitro in a vessel chamber. The inner and outer diameter of the arteries were measured by microangiometry, and spontenuous tone, wall thickness, wall cross-sectional area, tangential stress, incremental distensibility, circumferential incremental elastic modulus, thromboxane agonist-induced tone, and bradykinin-induced dilation were calculated.
  
  
  
  In hypertension, intramural small coronaries show inward eutrophic remodeling after ovariectomy comparing with hypertensive controls. Estrogen therapy had an opposite effect on vessel diameter. Hormone therapy led to an increase in spontaneous tone, allowing for greater dilatative capacity.
  
  
  
  Estrogen may therefore be considered to counterbalance some of the adverse changes seen in the wall of intramural coronaries in the early stages of chronic hypertension.
authors.affiliation: 1Institute of Human Physiology and Clinical Experimental Research 2Department of Orthopedics 3Department of Physiology 42nd Department of Internal Medicine-Department Section of Geriatrics 52nd Department of Obstetrics and Gynecology, Faculty of Medicine, Semmelweis University, Budapest, Hungary 6Department of Obstetrics and Gynecology, Meir Medical Center, Kfar Saba, affiliated with Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
authors.forename: Mate
authors.initials: M
authors.lastname: Matrai
authors.forename: Judit R
authors.initials: JR
authors.lastname: Hetthéssy
authors.forename: Gyorgy L
authors.initials: GL
authors.lastname: Nadasy
authors.forename: Bela
authors.initials: B
authors.lastname: Szekacs
authors.forename: Metin
authors.initials: M
authors.lastname: Mericli
authors.forename: Nandor
authors.initials: N
authors.lastname: Acs
authors.forename: Emil
authors.initials: E
authors.lastname: Monos
authors.forename: Nissim
authors.initials: N
authors.lastname: Arbib
authors.forename: Szabolcs
authors.initials: S
authors.lastname: Varbiro
mesh_terms: D000804:Angiotensin II; D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D003331:Coronary Vessels / Q000187:drug effects* / Q000473:pathology; D004195:Disease Models, Animal; D015914:Estrogen Replacement Therapy / Q000379:methods; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D006973:Hypertension / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology; D008593:Menopause; D010052:Ovariectomy; D051381:Rats; D017207:Rats, Sprague-Dawley; D066253:Vascular Remodeling / Q000187:drug effects*; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D004967:Estrogens; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000804:Angiotensin II; D001920:Bradykinin