Limitation of arteriolar myogenic activity by local nitric oxide: segment-specific effect of dietary salt

1999 ◽  
Vol 277 (5) ◽  
pp. H1946-H1955 ◽  
Author(s):  
Timothy R. Nurkiewicz ◽  
Matthew A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Salt Intake ◽  
Specific Effect ◽  
High Salt ◽  
Myogenic Response ◽  
Dietary Salt ◽  
No Donor ◽  
Spontaneously Hypertensive ◽  
High Salt Intake ◽  
Wistar Kyoto

The purpose of this study was to determine if local nitric oxide (NO) activity attenuates the arteriolar myogenic response in rat spinotrapezius muscle. We also investigated the possibility that hypertension, dietary salt, or their combination can alter any influence of local NO on the myogenic response. Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) fed low-salt (0.45%, LS) or high-salt (7%, HS) diets were enclosed in a ventilated airtight box with the spinotrapezius muscle exteriorized for intravital microscopy. Mean arterial pressure was unaffected by dietary salt in WKY but was significantly higher and augmented by dietary salt in SHR. In all experiments, elevation of microvascular pressure by box pressurization caused a 0–30% decrease in the diameter of large (arcade bridge) arterioles and a 21–27% decrease in the diameter of intermediate (arcade) arterioles. Inhibition of NO synthase with N G-monomethyl-l-arginine (l-NMMA) significantly enhanced myogenic responsiveness of arcade bridge arterioles in WKY-LS and SHR-LS but not in WKY-HS and SHR-HS.l-NMMA significantly enhanced the myogenic responsiveness of arcade arterioles in all four groups. Excess l-arginine reversed this effect of l-NMMA in all cases, and arteriolar responsiveness to the NO donor sodium nitroprusside was not different among the four groups. High-salt intake had no effect on the passive distension of arterioles in either strain during box pressurization. We conclude that 1) local NO normally attenuates arteriolar myogenic responsiveness in WKY and SHR, 2) dietary salt impairs local NO activity in arcade bridge arterioles of both strains, and 3) passive arteriolar distensibility is not altered by a high-salt diet in either strain.

Reactive oxygen species may contribute to reduced endothelium-dependent dilation in rats fed high salt

2000 ◽  
Vol 279 (1) ◽  
pp. H7-H14 ◽  
Author(s):  
Deborah M. Lenda ◽  
Bryan A. Sauls ◽  
Matthew A. Boegehold
Keyword(s):  
Reactive Oxygen Species ◽  
Salt Intake ◽  
Reactive Oxygen ◽  
High Salt ◽  
Oxygen Species ◽  
Dietary Salt ◽  
No Donor ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Salt Intake

In normotensive rats, an increase in dietary salt leads to decreased arteriolar responsiveness to acetylcholine (ACh) because of suppressed local nitric oxide (NO) activity. We evaluated the possibility that generation of reactive oxygen species in the arteriolar wall is responsible for this loss of NO activity. Arteriolar responses to iontophoretically applied ACh were examined in the superfused spinotrapezius muscle of Sprague-Dawley rats fed a low-salt (LS; 0.45%) or high-salt diet (HS; 7%) for 4–5 wk. Responses to ACh were significantly depressed in HS rats but returned to normal in the presence of the oxidant scavengers superoxide dismutase + catalase or 2,2,6,6-tetamethylpiperidine- N-oxyl (TEMPO) + catalase. Arteriolar responses to the NO donor sodium nitroprusside were similar in HS and LS rats. Arteriolar and venular wall oxidant activity, as determined by reduction of tetranitroblue tetrazolium, was significantly greater in HS rats than in LS rats. Exposure to TEMPO + catalase reduced microvascular oxidant levels to normal in HS rats. These data suggest that a high-salt diet leads to increased generation of reactive oxygen species in striated muscle microvessels, and this increased oxidative state may be responsible for decreased endothelium-dependent responses associated with high salt intake.

scholarly journals Dietary Salt With Nitric Oxide Deficiency Induces Nocturnal Polyuria via Hyperactivation of Intrarenal Angiotensin Ⅱ-SPAK-NCC Pathway

2021 ◽  
Author(s):  
Yosuke Sekii ◽  
Hiroshi Kiuchi ◽  
Kentaro Takezawa ◽  
Takahiro Imanaka ◽  
Sohei Kuribayashi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Salt Intake ◽  
Underlying Mechanism ◽  
High Salt ◽  
Common Disease ◽  
No Production ◽  
Nocturnal Polyuria ◽  
Dietary Salt ◽  
High Salt Intake

Abstract Nocturnal polyuria is the most frequent cause of nocturia, a common disease associated with a compromised quality of life and increased mortality. Its pathogenesis is complex, and the detailed underlying mechanism remains unknown. Herein, we report that concomitant intake of a high-salt diet and reduced nitric oxide (NO) production achieved through Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) administration in mice resulted in nocturnal polyuria recapitulating the clinical features in humans. High salt intake under reduced NO production overactivated the angiotensin II-SPAK (STE20/SPS1-related proline–alanine-rich protein kinase)-NCC (sodium chloride co-transporter) pathway in the kidney, resulting in the insufficient excretion of sodium during the day and its excessive excretion at night. Excessive Na excretion at night in turn leads to nocturnal polyuria due to osmotic diuresis. Our study identified a central role for the intrarenal angiotensin II-SPAK-NCC pathway in the pathophysiology of nocturnal polyuria, highlighting its potential as a promising therapeutic target.

Increases in CSF [Na+] precede the increases in blood pressure in Dahl S rats and SHR on a high-salt diet

2004 ◽  
Vol 287 (3) ◽  
pp. H1160-H1166 ◽  
Author(s):  
Bing S. Huang ◽  
Bruce N. Van Vliet ◽  
Frans H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
High Salt ◽  
Initial Increase ◽  
Primary Role ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Intracerebroventricular Infusion ◽  
High Salt Intake ◽  
Wistar Kyoto

In Dahl salt-sensitive (S) and salt-resistant (R) rats, and spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, at 5–6 wk of age, a cannula was placed in the cisterna magna, and cerebrospinal fluid (CSF) was withdrawn continuously at 75 μl/12 h. CSF was collected as day- and nighttime samples from rats on a regular salt intake (0.6% Na+; R-Na) and then on a high salt intake (8% Na+; H-Na). In separate groups of rats, the abdominal aorta was cannulated and blood pressure (BP) and heart rate (HR) measured at 10 AM and 10 PM, with rats first on R-Na and then on H-Na. On H-Na, CSF [Na+] started to increase in the daytime of day 2 in Dahl S rats and of day 3 in SHR. BP and HR did not rise until day 3 in Dahl S rats and day 4 in SHR. In Dahl R and WKY rats, high salt did not change CSF [Na+], BP, or HR. In a third set of Dahl S rats, sampling of both CSF and BP was performed in each individual rat. Again, significant increases in CSF [Na+] were observed 1–2 days earlier than the increases in BP and HR. In a fourth set of Dahl S rats, BP and HR were recorded continuously by means of radiotelemetry for 5 days on R-Na and 8 days on H-Na. On H-Na, BP (but not HR) increased first in the nighttime of day 2. In another set of Dahl S rats, intracerebroventricular infusion of antibody Fab fragments binding ouabain-like compounds (OLC) with high affinity prevented the increase in BP and HR by H-Na but further increased CSF [Na+]. Finally, in Wistar rats on H-Na, intracerebroventricular infusion of ouabain increased BP and HR but decreased CSF [Na+]. Thus, in both Dahl S and SHR on H-Na, increases in CSF [Na+] preceded the increases in BP and HR, consistent with a primary role of increased CSF [Na+] in the salt-induced hypertension. An increase in brain OLC in response to the initial increase in CSF [Na+] appears to attenuate further increases in CSF [Na+] but at the “expense” of sympathoexcitation and hypertension.

Effect of dietary salt on arteriolar nitric oxide in striated muscle of normotensive rats

1993 ◽  
Vol 264 (6) ◽  
pp. H1810-H1816 ◽  
Author(s):  
M. A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Striated Muscle ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Salt Intake ◽  
Low Salt ◽  
Induced Hypertension

This study evaluated the influence of high dietary salt intake on nitric oxide (NO) activity in the arteriolar network of rats resistant to salt-induced hypertension. The spinotrapezius muscle microvasculature was studied in inbred Dahl salt-resistant (SR/Jr) rats fed low (0.45%)- or high (7%)-salt diets for 4–5 wk. Arterial pressures were not different between groups at any time during the study. NO synthesis inhibition with NG-nitro-L-arginine-methyl ester (L-NAME) constricted arcade arterioles in low-salt SR/Jr and dilated arcade arterioles in high-salt SR/Jr. Arcade arteriole dilation to acetylcholine (ACh), but not sodium nitroprusside (SNP), was impaired in high-salt SR/Jr. In contrast, transverse and distal arteriole responses to L-NAME, ACh, and SNP were identical in high- and low-salt SR/Jr. These findings indicate that high salt intake, in the absence of increased arterial pressure, suppresses the influence of basal and evoked NO on vascular tone in arcading arterioles, but not in smaller transverse and distal arterioles. Unaltered SNP responses in high-salt SR/Jr suggest that this effect does not involve a change in arteriolar smooth muscle responsiveness to NO.

Salt loading augments vascular responses to indomethacin in stroke-prone SHR

1982 ◽  
Vol 243 (3) ◽  
pp. H360-H364
Author(s):  
T. Imaizumi ◽  
A. Takeshita ◽  
T. Ashihara ◽  
M. Nakamura
Keyword(s):  
Vascular Resistance ◽  
Prostaglandin E1 ◽  
Salt Intake ◽  
High Salt ◽  
Salt Loading ◽  
Salt Diet ◽  
Spontaneously Hypertensive ◽  
High Salt Intake ◽  
Endogenous Prostaglandins ◽  
Wistar Kyoto

We examined whether endogenous prostaglandins (PGs) participated in control of hindquarters vascular resistance during salt loading in stroke-prone spontaneously hypertensive rates (SHR-SP). SHR-SP and Wistar-Kyoto rats (WKY) were fed either a normal (0.3% NaCl) or high (8% NaCl) salt diet for 5 wk. High salt increased blood pressure and hindquarter vascular resistance (VR) in SHR-SP (P less than 0.01) but not in WKY. Indomethacin given intravenously increased hindquarter VR in SHR-SP during high salt as well as during normal salt (P less than 0.01) but not in either group of WKY. In SHR-SP the increase in hindquarter VR by PG synthesis inhibitors were two times greater during high salt than during normal salt (P less than 0.01). In addition, hindquarter vasodilatation by bradykinin was greater (P less than 0.05) in SHR-SP during high salt than that during normal salt, but vasodilatation by prostaglandin E1 or nitroglycerin was not different between the two groups. These results suggest that vascular synthesis of endogenous PGs was greater in SHR-SP during high salt than that during normal salt. Increased endogenous PGs may play an important role in the regulation of hindquarter VR during high salt intake in SHR-SP.

scholarly journals A preliminary study of the effect of a high-salt diet on transcriptome dynamics in rat hypothalamic forebrain and brainstem cardiovascular control centers

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8528
Author(s):  
Chitra Devi Ramachandran ◽  
Khadijeh Gholami ◽  
Sau Kuen Lam ◽  
See Ziau Hoe
Keyword(s):  
Regulatory Networks ◽  
Salt Intake ◽  
Brain Regions ◽  
High Salt ◽  
Ventrolateral Medulla ◽  
Dietary Salt ◽  
Spontaneously Hypertensive ◽  
Dietary Salt Intake ◽  
Expression Of Genes ◽  
Wistar Kyoto

Background High dietary salt intake is strongly correlated with cardiovascular (CV) diseases and it is regarded as a major risk factor associated with the pathogenesis of hypertension. The CV control centres in the brainstem (the nucleus tractus solitarii (NTS) and the rostral ventrolateral medulla (RVLM)) and hypothalamic forebrain (the subfornical organ, SFO; the supraoptic nucleus, SON and the paraventricular nucleus, PVN) have critical roles in regulating CV autonomic motor outflows, and thus maintaining blood pressure (BP). Growing evidence has implicated autonomic regulatory networks in salt-sensitive HPN (SSH), but the genetic basis remains to be delineated. We hypothesized that the development and/ or maintenance of SSH is reliant on the change in the expression of genes in brain regions controlling the CV system. Methodology We used RNA-Sequencing (RNA-Seq) to describe the differential expression of genes in SFO, SON, PVN, NTS and RVLM of rats being chronically fed with high-salt (HS) diet. Subsequently, a selection of putatively regulated genes was validated with quantitative reverse transcription polymerase chain reaction (qRT-PCR) in both Spontaneously Hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats. Results The findings enabled us to identify number of differentially expressed genes in SFO, SON, PVN, NTS and RVLM; that are either up-regulated in both strains of rats (SON- Caprin2, Sctr), down-regulated in both strains of rats (PVN- Orc, Gkap1), up-regulated only in SHRs (SFO- Apopt1, Lin52, AVP, OXT; SON- AVP, OXT; PVN- Caprin2, Sclt; RVLM- A4galt, Slc29a4, Cmc1) or down-regulated only in SHRs (SON- Ndufaf2, Kcnv1; PVN- Pi4k2a; NTS- Snrpd2l, Ankrd29, St6galnac6, Rnf157, Iglon5, Csrnp3, Rprd1a; RVLM- Ttr, Faim). Conclusions These findings demonstrated the adverse effects of HS diet on BP, which may be mediated via modulating the signaling systems in CV centers in the hypothalamic forebrain and brainstem.

High-salt diet depresses acetylcholine reactivity proximal to NOS activation in cerebral arteries

2002 ◽  
Vol 283 (1) ◽  
pp. H353-H363 ◽  
Author(s):  
Francis A. Sylvester ◽  
David W. Stepp ◽  
Jefferson C. Frisbee ◽  
Julian H. Lombard
Keyword(s):  
Salt Intake ◽  
Cerebral Arteries ◽  
High Salt ◽  
Receptor Expression ◽  
Dietary Salt ◽  
No Donor ◽  
Dietary Salt Intake ◽  
No Release ◽  
Type 3 ◽  
Cytochrome P 450

Rats were fed a low-salt (LS; 0.4% NaCl) or high-salt (HS; 4.0% NaCl) diet for 3 days, and the responses of isolated cerebral arteries to acetylcholine (ACh), the nitric oxide (NO)-dependent dilator bradykinin, and the NO donor 6-(2-hydroxy-1-methyl-2-nitrosohydrazino)- N-methyl-1-hex-anamine (NOC-9) were determined. ACh-induced vasodilation and NO release, assessed with the fluorescent NO indicator 4,5-diaminofluorescein (DAF-2) diacetate, were eliminated with the HS diet. Inhibition of cyclooxygenase, cytochrome P-450 epoxygenase, and acetylcholinesterase did not alter ACh responses. Bradykinin and NOC-9 caused a similar dilation in cerebral arteries of all groups. Arteries from animals on LS or HS diets exhibited similar levels of basal superoxide (O[Formula: see text]) production, assessed by dihydroethidine fluorescence, and ACh responses were unaffected by O[Formula: see text] scavengers. Muscarinic type 3 receptor expression was unaffected by dietary salt intake. These results indicate that 1) a HS diet attenuates ACh reactivity in cerebral arteries by inhibiting NO release, 2) this attenuation is not due to production of a cyclooxygenase-derived vasoconstrictor or elevated O[Formula: see text] levels, and 3) alteration(s) in ACh signaling are located upstream from NO synthase.

scholarly journals Effects of spironolactone in spontaneously hypertensive adult rats subjected to high salt intake

Clinics ◽  
2011 ◽  
Vol 66 (3) ◽  
pp. 477-482 ◽  
Author(s):  
Marcelo Perim Baldo ◽  
Divanei Zaniqueli ◽  
Ludimila Forechi ◽  
Rebeca Caldeira Machado ◽  
Sérgio Lamêgo Rodrigues ◽  
...  
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Adult Rats ◽  
Spontaneously Hypertensive ◽  
High Salt Intake
Sign in / Sign up

Export Citation Format

Share Document