Plasma ANP and cyclic GMP after physical exercise in patients with mitral valve disease and in healthy subjects

Radziszewski, Waldemar; Surdacki, Andrzej; Vuorinen, Pauli; Vapaatalo, Heikki; Saari, Marisanna; Uusitalo, Arja; Ruskoaho, Heikki; Dubiel, Jacek S.; Gryglewski, Ryszard J.

doi:10.1016/0167-5273(93)90002-x

Cited by 4 publications

(2 citation statements)

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“…NO acts through the stimulation of the soluble form of guanylate cyclase (GC) in target cells, inducing an increase in the intracellular concentration of cGMP [3]. Dynamic exercise is known to produce an increase in ANP in healthy subjects and in patients [4]. Dynamic exercise is known to produce an increase in ANP in healthy subjects and in patients [4].…”

Section: Introductionmentioning

confidence: 99%

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Contribution of nitric oxide to exercise‐induced changes in healthy volunteers: effects of acute exercise and long‐term physical training

Poveda¹,

Riestra²,

Salas³

et al. 1997

Eur J Clin Investigation

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Endothelium plays a central role in the regulation of regional blood flow through the release of certain vasoactive substances. We conducted this study to test whether an increase in the production of nitric oxide (NO) metabolites, atrial natriuretic peptide (ANP) and plasma and intraplatelet cyclic guanosine 3':5' monophosphate (cGMP) is involved in the adaptation to chronic exercise in physically trained people and in the vasodilatation induced by acute physical exercise. We studied one group of 10 trained athletes and another group of 10 untrained people. We measured plasma levels of nitrites, nitrates and cGMP and intraplatelet levels of cGMP, as an indicator of intracellular guanylate cyclase activity, and ANP before and after a maximal treadmill test. Resting cardiac rate (CR) and systolic blood pressure (SBP) were lower in the athlete group than in the control group (73.8 +/- 3.6 vs. 92 +/- 5.9; P < 0.02 and 110 +/- 2.58 vs. 118 +/- 3.27; P < 0.02 respectively). SBP did not show differences between groups after the exercise test. Diastolic blood pressure (DBP) at rest was lower in the athlete group (71 +/- 1.79 vs. 80.5 +/- 3.53; P < 0.03) and the decrease after maximal exercise was more pronounced in this group (64 +/- 2.67 vs. 74.5 +/- 3.2; P < 0.02). Basal plasma nitrites were 4.9 +/- 0.8 in the athlete group and 1.9 +/- 0.3 in the control group (P < 0.05). After exercise, test differences between groups remained (P < 0.05). Nitrates were significantly higher in the group of athletes and did not show exercise-related changes. Plasma levels of cGMP and ANP increased in both groups after the treadmill test, with no differences between groups. Among the athletes, cGMP increased from 1.11 +/- 0.1 to 2.6 +/- 0.4 (P < 0.001), whereas in the untrained group plasma cGMP rose from 1.14 +/- 0.09 to 1.86 +/- 0.2 (P < 0.01). There was a significant correlation between the increases in plasma cGMP and the atrial natriuretic peptide in both groups (r = 0.91, P < 0.0002, for athletes; and r= 0.68, P < 0.04, for control group). The intraplatelet concentration of cGMP did not show differences between groups and did not change after exercise. In conclusion, we have found increased basal levels of plasma nitrite and nitrate in trained subjects. Exercise does not produce differences in the increments of these metabolites. Therefore, we speculate the release of nitric oxide is not augmented by exercise in trained athletes.

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Section: Introductionmentioning

confidence: 99%

“…This nucleotide, acting as a second messenger, produces smooth muscle relaxation and vasodilatation. Dynamic exercise is known to produce an increase in ANP in healthy subjects and in patients [4]. ANP induces vasodilatation through the stimulation of particulate GC, and plasma cGMP is a good clinical indicator of ANP secretion [5].…”

Section: Introductionmentioning

confidence: 99%