Literature DB >> 2940119

Cardiovascular effects of atrial natriuretic extract in the whole animal.

U Ackermann.   

Abstract

Atrial tissue extract (AE) and ventricular tissue extract cause identical decreases in total peripheral resistance when they are injected i.v. into anesthetized rats. However, only AE causes significant hypotension because of cardiac inhibition. This involves both bradycardia and failure of stroke volume to increase appropriately. The observations cannot be explained by direct action of AE on myocytes, but are more likely to be the result of interactions with cardiovascular reflex mechanisms. Excitation of chemosensitive cardiac receptors with vagal afferents appears to be an important afferent mechanism. The efferent limb for the negative chronotropic response resides partly in the vagus nerves and partly in cardiac sympathetic nerves. The negative inotropic response of AE was not altered by vagotomy, spinal section, atropine, or propranolol. These results suggest that atrial peptides may cause the release of a negatively inotropic substance from a site that is not yet identified.

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Year:  1986        PMID: 2940119

Source DB:  PubMed          Journal:  Fed Proc        ISSN: 0014-9446


  3 in total

1.  Expression of the atrial natriuretic peptide gene in the cardiac muscle of rat extrapulmonary and intrapulmonary veins.

Authors:  D R Springall; M Bhatnagar; J Wharton; Q Hamid; S Gulbenkian; M Hedges; L Meleagros; S R Bloom; J M Polak
Journal:  Thorax       Date:  1988-01       Impact factor: 9.139

2.  Vitamin D receptors in heart: effects on atrial natriuretic factor.

Authors:  H J Bidmon; J Gutkowska; R Murakami; W E Stumpf
Journal:  Experientia       Date:  1991-09-15

3.  Effects of expansion of blood volume and bilateral vagotomy on specific heart granules and release of atrial natriuretic peptide in the rat.

Authors:  J N Skepper; V Navaratnam; N D Martensz
Journal:  Cell Tissue Res       Date:  1989-10       Impact factor: 5.249

  3 in total

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