title: [Changes of right atrial myoendocrine cells during hypertension and after arterial pressure decrease].
abstract: It is well known now that atrial cardiomyocytes carry out both contractile and endocrine activities--they synthesize, accumulate in specific secretory granules and release the natriuretic peptides. The main physiological effects of natriuretic peptides are antagonistic to the renin-angiotensin-aldostrol system, but their role in the development of hypertension is still disputable. The aim of this investigation is to estimate using electron microscopy the secretory activities of atrial myoendocrine cells in rats with inherited stress-induced arterial hypertension (ISIAH stain). It has been shown that myoendocrine cells in the ISIAH rats with arterial pressure about 180 mm Hg reveal morphological features of increased synthesis, extra accumulation and release of natriuretic peptides compared with normotensive control rats. In the ISIAH rats treated with losartan (angiotensin II receptor blocker) and therefore having a sustained decrease in arterial pressure to 140 mm Hg, changes in granular pool composition, reduction of the number and diameter of the secretory granules, reduction of Golgi complexes, and increased intracellular degradation of secretory stores were found in the myoendocrine cells. At the same time the marked capillary hyperemia and interstitial edema in the myocardium were observed. Thus, in rats with severe inherited hypertension, the secretory activity of heart myoendocrine cells is sharply increased and directly depends on the arterial blood pressure level. This proves that natriuretic peptides actively participate in the regulation of hemodynamics during with cardiovascular pathology.
authors.forename: V F
authors.initials: VF
authors.lastname: Maksimov
authors.forename: I M
authors.initials: IM
authors.lastname: Korostyshevskaia
authors.forename: S A
authors.initials: SA
authors.lastname: Kurganov
authors.forename: A L
authors.initials: AL
authors.lastname: Markel'
authors.forename: N S
authors.initials: NS
authors.lastname: Rudenko
authors.forename: G S
authors.initials: GS
authors.lastname: Iakobson
mesh_terms: D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D009320:Atrial Natriuretic Factor / Q000096:biosynthesis / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects; D006056:Golgi Apparatus / Q000187:drug effects / Q000648:ultrastructure; D006325:Heart Atria / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D022142:Secretory Vesicles / Q000187:drug effects / Q000648:ultrastructure
chemical_list: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D009320:Atrial Natriuretic Factor; D019808:Losartan