Central venous pressure – a physiological stimulus for secretion of atrial natriuretic peptide in humans?

Schütten, H. J.; Johannessen, Arne; Torp-Pedersen, C.; Sander‐Jensen, K.; Bie, Peter; Warberg, Jørgen

doi:10.1111/j.1748-1716.1987.tb08236.x

Cited by 75 publications

(47 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A specific antibody (AB95069/5) produced in this laboratory was used in a final dilution of 1:27,000 according to the procedure of Schü tten et al (31). The detection limit was 1.5 pg/ml, and the mean recovery of unlabeled atrial natriuretic peptide (ANP) added to plasma before extraction was 74%.…”

Section: Methodsmentioning

confidence: 99%

Volume expansion during acute angiotensin II receptor (AT₁) blockade and NOS inhibition in conscious dogs

Andersen

Sandgaard

Bie

2002

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

The responses to AT1-receptor blockade (candesartan 1 mg/kg) and to concomitant volume expansion (saline 35 ml/kg for 90 min) with and without nitric oxide synthase (NOS) ) were investigated in separate experiments in normal dogs. AT1 blockade decreased arterial pressure (106 Ϯ 4 to 96 Ϯ 5 mmHg) and increased glomerular filtration rate (GFR) by 17% and sodium excretion threefold. NOS inhibition increased arterial pressure (103 Ϯ 3 to 116 Ϯ 3 mmHg) and decreased GFR by 21% and reduced sodium excretion by some 80%. Volume expansion increased arterial pressure significantly in all series involving this procedure, most pronounced during combined AT1 blockade and NOS inhibition (21 Ϯ 4 mmHg). Volume expansion during AT 1 blockade elicited marked natriuresis (26 Ϯ 11 to 274 Ϯ 55 mol/min) that was severely reduced by concomitant NOS inhibition (10 Ϯ 3 to 45 Ϯ 11 mol/min), but still much larger than that seen with volume expansion during NOS inhibition alone (2 Ϯ 1 to 23 Ϯ 7 mol/min). Volume expansion during AT 1 blockade increased GFR (ϩ30%), less so during combined AT1 blockade and NOS inhibition (ϩ13%), but it did not increase GFR significantly (P ϭ 0.07) during NOS inhibition alone. Plasma ANG II increased greater than sevenfold with AT 1 blockade and doubled with NOS inhibition (paired t-test, P Ͻ 0.05), whereas it decreased by 50-80% during volume expansion irrespective of pretreatment, i.e., during NOS inhibition, volume expansion did not generate subnormal plasma ANG II concentrations. In conclusion, 1) acute AT 1 blockade leads to hyperfiltration, natriuresis, and hyperresponsiveness to volume expansion, 2) these responses are Ͼ85% inhibitable by unspecific NOS inhibition, and 3) NOS inhibition alone is followed by increases in plasma ANG II, hypofiltration, and severe antinatriuresis that may be counterbalanced but not overwhelmed by volume expansion. Thus NOS inhibition virtually abolishes the volume expansion natriuresis, at least in part, due to the lack of appropriate inhibition of the renin-angiotensin-aldosterone system. sodium excretion; blood pressure; glomerular filtration rate; N G -nitro-L-arginine methyl ester; candesartan THE CONTROL OF RENAL SODIUM excretion is multifactorial, involving physical, neural, and humoral mechanisms. However, the relative contributions of the individual components are still unclear, e.g., evaluation of the importance of the renin-angiotensin system vs. the role of nitric oxide (NO) in renal sodium homeostasis is particularly complex. The natriuretic effect of volume expansion is linked to a decrease in plasma levels of ANG II (e.g., 3, 32), and an intact NO synthesis is also a prerequisite for volume expansion natriuresis (21, 26). However, the relative importance and possible interaction between the two systems are poorly elucidated in conscious animals. We recently demonstrated (2) that a slow, moderate volume expansion in the absence of ANG II (due to converting enzyme inhibition) elicited a marked exaggeration of the natriuresis seen in control dogs, although blo...

show abstract

Section: Methodsmentioning

confidence: 99%

Volume expansion during acute angiotensin II receptor (AT₁) blockade and NOS inhibition in conscious dogs

Andersen

Sandgaard

Bie

2002

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…A specific antibody (AB95069/5) produced in this laboratory was used in a final dilution of 1:27,000 according to the procedure of Schü tten et al (32). The detection limit was 1.5 pg/ml, and the mean recovery of unlabeled atrial natriuretic peptide (ANP) added to plasma before extraction was 78%.…”

Section: Methodsmentioning

confidence: 99%

Volume expansion during NOS substrate donation with l-arginine: regulatory offsetting of renal response?

Andersen

Sandgaard

Bie

2002

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Ϫ1 ⅐ min Ϫ1 ) and to slow volume expansion (saline 35 ml/kg for 90 min) alone and in combination were investigated in separate experiments. L-Arginine left blood pressure and plasma ANG II unaffected but decreased heart rate (6 Ϯ 2 beats/min) and urine osmolality, increased glomerular filtration rate (GFR) transiently, and caused sustained increases in sodium excretion (fourfold) and urine flow (0.2 Ϯ 0.0 to 0.7 Ϯ 0.1 ml/min). Volume expansion increased arterial blood pressure (102 Ϯ 3 to 114 Ϯ 3 mmHg), elevated GFR persistently by 24%, and enhanced sodium excretion to a peak of 251 Ϯ 31 mol/min, together with marked increases in urine flow, osmolar and free water clearances, whereas plasma ANG II decreased (8.1 Ϯ 1.7 to 1.6 Ϯ 0.3 pg/ml). Combined volume expansion and L-arginine infusion tended to increase arterial blood pressure and increased GFR by 31%, whereas peak sodium excretion was enhanced to 335 Ϯ 23 mol/min at plasma ANG II levels of 3.0 Ϯ 1.1 pg/ml; urine flow and osmolar clearance were increased at constant free water clearance. In conclusion, L-arginine 1) increases sodium excretion, 2) decreases basal urine osmolality, 3) exaggerates the natriuretic response to volume expansion by an average of 50% without persistent changes in GFR, and 4) abolishes the increase in free water clearance normally occurring during volume expansion. Thus L-arginine is a natriuretic substance compatible with a role of nitric oxide in sodium homeostasis, possibly by offsetting/shifting the renal response to sodium excess. sodium excretion; free water clearance; angiotensin PHYSICAL, NEURAL, AND HUMORAL mechanisms are involved in the control of renal sodium excretion. However, the relative influence of each of the components is still controversial, and the evaluation of the importance of the renin-angiotensin system vs. the role of nitric oxide (NO) in renal sodium homeostasis is particularly complex. The natriuretic effect of volume expansion is linked to a decrease in plasma levels of ANG II (e.g., 2, 5), and an intact NO synthesis is also a prerequisite for volume expansion natriuresis (e.g., 3). However, the relative importance and possible interaction between the two systems are poorly elucidated.NO is a potent renal vasodilator and natriuretic substance synthesized in the kidney (14,15,27,31,33,36). It has been shown that acute and chronic elevations in extracellular fluid volume lead to increased NO synthesis (9,16,26,29). Conversion of L-arginine into the vasorelaxant NO takes place in endothelial cells in response to a variety of stimuli by the enzyme NO synthase (NOS). In a recent study in dogs (3), we blocked the NOS unspecifically using the structural analog N G -nitro-L-arginine methyl ester (L-NAME) and demonstrated that this NOS inhibition is followed by increases in plasma ANG II, renal hypofiltration, and severe antinatriuresis that may be no more than returned to control levels by a sizeable volume expansion (3.5% body wt). Thus NOS inhibition virtually abolishes the volume expansion natriuresis, and thi...

show abstract

“…We have put up a hypothesis on the pathophysiological role of ANP in preeclampsia. ANP is released from atrial myocytes in response to increased atrial pressure (Schutten et al 1987). In preeclapmsia, we speculate that the atrial pressure may increase by many factors, viz.…”

Section: Resultsmentioning

confidence: 99%

Maternal and Fetal Atrial Natriuretic Peptide Levels, Maternal Plasma Renin Activity, Angiotensin II, Prostacyclin and Thromboxane A2 Levels in Normal and Preeclamptic Pregnancies.

Furuhashi

Tsujiei²,

Kimura³

et al. 1991

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

To clarify the possible role of elevated atrial natriuretic peptide (ANP) in the pathophysiology of preeclapmsia, we measured ANP, renin activity (PRA), angiotensin II (Ang II), TXB2 (a stable metabolite of TXA2) and 6-keto-PGFIa (a stable end product of PGI2) concentrations in the plasma of 19 normal pregnant women and 35 severe preeclamptic patients at term. Plasma ANP levels in the preeclamptic patients (n = 35, 71.5 + 3.8 pg/ml, mean+ s.E.) and also umbilical plasma ANP (n = 35, 83.0± 4.2 pg/ml) were significantly (p <0.01) higher than those of normal pregnant women plasma (n=19, 58.7± 3.7 pg/ml) and umbilical plasma (n =19, 47.6±4.7 pg/ml ). There was a significant (p <0.01) positive correlation between maternal ANP levels and fetal ANP levels (n = 54, r = 0.44). Plasma PRA and 6-keto-PGFIa levels in preeclampsia were significantly (p <0.05) lower than those of normal pregnancy. The ratio of 6-keto-PGFIa/TXB2 in preeclampsia was significantly (p <0.01) lower than that of normal pregnancy as we reported previously. There was no significant correlation between plasma ANP level and plasma PRA, Ang II, plasma TXB2 and 6-keto-PGFI a concentrations. Moreover there was no significant correlation between plasma ANP level and the severity of preeclampsia. These data suggest the possibility of a transplacental crossing of ANP secreted by feto-placental unit, which might be, at least in part, responsible for the high ANP levels observed in preeclampsia. The ANP in preeclampsia is not related directly to hypertension, but it may play a substantial role in the regulation or normalization of blood volume and vascular reactivity.atrial natriuretic peptide ; plasma renin activity ; preeclampsia ; Prostacyclin ; thromboxane A2 Atrial natriuretic peptide (ANP) is a peptide, synthesized and released from

show abstract

Central venous pressure – a physiological stimulus for secretion of atrial natriuretic peptide in humans?

Cited by 75 publications

References 28 publications

Volume expansion during acute angiotensin II receptor (AT₁) blockade and NOS inhibition in conscious dogs

Volume expansion during acute angiotensin II receptor (AT₁) blockade and NOS inhibition in conscious dogs

Volume expansion during NOS substrate donation with l-arginine: regulatory offsetting of renal response?

Maternal and Fetal Atrial Natriuretic Peptide Levels, Maternal Plasma Renin Activity, Angiotensin II, Prostacyclin and Thromboxane A2 Levels in Normal and Preeclamptic Pregnancies.

Contact Info

Product

Resources

About

Central venous pressure – a physiological stimulus for secretion of atrial natriuretic peptide in humans?

Cited by 75 publications

References 28 publications

Volume expansion during acute angiotensin II receptor (AT1) blockade and NOS inhibition in conscious dogs

Volume expansion during acute angiotensin II receptor (AT1) blockade and NOS inhibition in conscious dogs

Volume expansion during NOS substrate donation with l-arginine: regulatory offsetting of renal response?

Maternal and Fetal Atrial Natriuretic Peptide Levels, Maternal Plasma Renin Activity, Angiotensin II, Prostacyclin and Thromboxane A2 Levels in Normal and Preeclamptic Pregnancies.

Contact Info

Product

Resources

About

Volume expansion during acute angiotensin II receptor (AT₁) blockade and NOS inhibition in conscious dogs

Volume expansion during acute angiotensin II receptor (AT₁) blockade and NOS inhibition in conscious dogs