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2017 ; 203
(ä): 58-66
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Hepatic and renal mechanisms underlying the osmopressor response
#MMPMID28143710
Mai TH
; Garland EM
; Diedrich A
; Robertson D
Auton Neurosci
2017[Mar]; 203
(ä): 58-66
PMID28143710
show ga
Increased blood pressure (BP) is observed in patients with impaired baroreflexes
after water drinking. The stimulus for this effect is low blood osmolality, and
it has been termed the osmopressor response (OPR). The BP increase is associated
with activation of the sympathetic nervous system and a requirement for transient
receptor potential vanilloid 4 (TRPV4) channels. However, the mechanisms
underlying the OPR are poorly understood. We tested the hypothesis that
hypotonicity is sensed in the portal area to initiate the OPR. Sino-aortic
denervated mice were used and BP was monitored for 30min after fluid infusion
while mice were under anesthesia. Infusion of hypotonic fluid (0.45% saline), but
not of isotonic 0.9% saline, directly into the portal vein, produced an immediate
OPR (increase in BP with saline 0.45%: 15±13 vs. 0.9%: -7±2mmHg, p=0.003; AUC:
0.45%: 150±99, n=7 vs. 0.9%: -74±60mmHg·min, n=5, p=0.003). However, 0.45% saline
was not able to trigger a similar response in TRPV4(-/-) mice (?BP(TRPV4):
-2±5mmHg, n=8, p=0.009). Hypotonic saline did not raise BP when infused at the
same speed and volume into the jugular vein (jugular: -5±6mmHg, p=0.002, compared
to portal). Denervation of the splanchnic nerve by celiac ganglionectomy (CGX)
did not abolish the OPR (CGX: 15±11 vs. Sham: 16±6mmHg, p=0.34). Renal
denervation diminished the OPR elicited by duodenal water infusion (denervation:
9±4 vs. sham: 31±15mmHg, p=0.016). Therefore, hypotonicity in the portal
circulation, probably sensed by TRPV4 channels, triggers the OPR and intact renal
nerves are needed for the full response.
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