Renal denervation modulates angiotensin receptor expression in the renal cortex of rabbits with chronic heart failure

Excessive sympathetic drive is a hallmark of chronic heart failure (HF). Disease progression can be correlated with plasma norepinephrine concentration. Renal function is also correlated with disease progression and prognosis. Because both the renal nerves and renin-angiotensin II system are activat...

Celý popis

Uloženo v:
Podrobná bibliografie
Vydáno v:American journal of physiology. Renal physiology Ročník 300; číslo 1; s. F31
Hlavní autoři: Clayton, Sarah C, Haack, Karla K V, Zucker, Irving H
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 01.01.2011
Témata:
Animals
Denervation
Heart Failure - physiopathology
Kidney - innervation
Kidney - metabolism
Kidney Cortex - metabolism
Male
Norepinephrine - metabolism
Rabbits
Receptor, Angiotensin, Type 1 - biosynthesis
Receptor, Angiotensin, Type 2 - biosynthesis
Receptors, Angiotensin - biosynthesis
Renal Circulation - drug effects
Smoke - adverse effects
Vascular Resistance - drug effects
ISSN:1522-1466, 1522-1466
On-line přístup:Zjistit podrobnosti o přístupu
Tagy: Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
Popis
Shrnutí:Excessive sympathetic drive is a hallmark of chronic heart failure (HF). Disease progression can be correlated with plasma norepinephrine concentration. Renal function is also correlated with disease progression and prognosis. Because both the renal nerves and renin-angiotensin II system are activated in chronic HF we hypothesized that excessive renal sympathetic nerve activity decreases renal blood flow in HF and is associated with changes in angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R) expression. The present study was carried out in conscious, chronically instrumented rabbits with pacing-induced HF. We found that rabbits with HF showed a decrease in mean renal blood flow (19.8±1.6 in HF vs. 32.0±2.5 ml/min from prepace levels; P<0.05) and an increase in renal vascular resistance (3.26±0.29 in HF vs. 2.21±0.13 mmHg·ml(-1)·min in prepace normal rabbits; P<0.05) while the blood flow and resistance was not changed in HF rabbits with the surgical renal denervation. Renal AT1R expression was increased by ∼67% and AT2R expression was decreased by ∼87% in rabbits with HF; however, kidneys from denervated rabbits with HF showed a near normalization in the expression of these receptors. These results suggest renal sympathetic nerve activity elicits a detrimental effect on renal blood flow and may be associated with alterations in the expression of angiotensin II receptors.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1522-1466
1522-1466
DOI:10.1152/ajprenal.00088.2010