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Sympathetic overactivity prevails over the vascular amplifier phenomena in a chronic kidney disease rat model of hypertension.

Ameer OZ, Hildreth CM, Phillips JK - Physiol Rep (2014)

Bottom Line: In LPK, the ratio of the hexamethonium/vasodilator MAP responses was greater when compared with Lewis (hexamethonium/SNP 1.34 ± 0.1 vs. 0.9 ± 0.09 and hexamethonium/adenosine: 2.28 ± 0.3 vs. 1.16 ± 0.1, both P < 0.05) but not SHR.The slope of the relationship between the fall in SBP induced by hexamethonium and normalized low frequency (LFnu) power was also greater in the LPK (17.93 ± 3.26 mmHg/LFnu) compared with Lewis (2.78 ± 0.59 mmHg/LFnu, P = 0.001) and SHR (3.36 ±0.72 mmHg/LFnu, P = 0.003).These results indicate that in the LPK, sympathetic activity predominates over any vascular amplifier effect, supporting increased sympathetic vasomotor tone as a major contributor to hypertension in this model of CKD.

View Article: PubMed Central - PubMed

Affiliation: The Australian School of Advanced Medicine, Macquarie University, Sydney, New South Wales, Australia.

No MeSH data available.


Related in: MedlinePlus

Dose dependent effects of sodium nitroprusside (SNP; A), adenosine (B) and the ganglionic blocker hexamethonium (C) on systolic blood pressure (SBP) in Lewis, Lewis polycystic kidney (LPK) and spontaneously hypertensive rats (SHR). Results are expressed as mean ± SEM. *P <0.05 compared to Lewis and #P <0.05 compared to SHR for individual doses as indicated.
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fig02: Dose dependent effects of sodium nitroprusside (SNP; A), adenosine (B) and the ganglionic blocker hexamethonium (C) on systolic blood pressure (SBP) in Lewis, Lewis polycystic kidney (LPK) and spontaneously hypertensive rats (SHR). Results are expressed as mean ± SEM. *P <0.05 compared to Lewis and #P <0.05 compared to SHR for individual doses as indicated.

Mentions: In response to administration of SNP, the two‐way ANOVA identified both a dose‐ and strain‐dependent effect on MAP and SBP (P <0.001). This was evident as a dose‐dependent reduction in all strains (Figs. 1A, 2A). In the Lewis, maximal depressor responses to SNP were observed following 10 μg/kg for both MAP and SBP; whereas, in the LPK and SHR, maximal depressor responses to SNP (MAP and SBP) were seen with 20 μg/kg. The overall response in the LPK was significantly greater than that in the Lewis for both MAP and SBP. No differences were identified between LPK and SHR at any dose of SNP. Hemodynamic responses to SNP at 20 μg/kg are presented in Table 2. At this dose, there was also a significant difference in the PP response between the LPK versus Lewis rats. Absolute values are provided in Table 3.


Sympathetic overactivity prevails over the vascular amplifier phenomena in a chronic kidney disease rat model of hypertension.

Ameer OZ, Hildreth CM, Phillips JK - Physiol Rep (2014)

Dose dependent effects of sodium nitroprusside (SNP; A), adenosine (B) and the ganglionic blocker hexamethonium (C) on systolic blood pressure (SBP) in Lewis, Lewis polycystic kidney (LPK) and spontaneously hypertensive rats (SHR). Results are expressed as mean ± SEM. *P <0.05 compared to Lewis and #P <0.05 compared to SHR for individual doses as indicated.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255812&req=5

fig02: Dose dependent effects of sodium nitroprusside (SNP; A), adenosine (B) and the ganglionic blocker hexamethonium (C) on systolic blood pressure (SBP) in Lewis, Lewis polycystic kidney (LPK) and spontaneously hypertensive rats (SHR). Results are expressed as mean ± SEM. *P <0.05 compared to Lewis and #P <0.05 compared to SHR for individual doses as indicated.
Mentions: In response to administration of SNP, the two‐way ANOVA identified both a dose‐ and strain‐dependent effect on MAP and SBP (P <0.001). This was evident as a dose‐dependent reduction in all strains (Figs. 1A, 2A). In the Lewis, maximal depressor responses to SNP were observed following 10 μg/kg for both MAP and SBP; whereas, in the LPK and SHR, maximal depressor responses to SNP (MAP and SBP) were seen with 20 μg/kg. The overall response in the LPK was significantly greater than that in the Lewis for both MAP and SBP. No differences were identified between LPK and SHR at any dose of SNP. Hemodynamic responses to SNP at 20 μg/kg are presented in Table 2. At this dose, there was also a significant difference in the PP response between the LPK versus Lewis rats. Absolute values are provided in Table 3.

Bottom Line: In LPK, the ratio of the hexamethonium/vasodilator MAP responses was greater when compared with Lewis (hexamethonium/SNP 1.34 ± 0.1 vs. 0.9 ± 0.09 and hexamethonium/adenosine: 2.28 ± 0.3 vs. 1.16 ± 0.1, both P < 0.05) but not SHR.The slope of the relationship between the fall in SBP induced by hexamethonium and normalized low frequency (LFnu) power was also greater in the LPK (17.93 ± 3.26 mmHg/LFnu) compared with Lewis (2.78 ± 0.59 mmHg/LFnu, P = 0.001) and SHR (3.36 ±0.72 mmHg/LFnu, P = 0.003).These results indicate that in the LPK, sympathetic activity predominates over any vascular amplifier effect, supporting increased sympathetic vasomotor tone as a major contributor to hypertension in this model of CKD.

View Article: PubMed Central - PubMed

Affiliation: The Australian School of Advanced Medicine, Macquarie University, Sydney, New South Wales, Australia.

No MeSH data available.


Related in: MedlinePlus