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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

Ratio of the mean arterial pressure (MAP) response after ganglionic blockade (hexamethonium 8 mg/kg i.v.) to that of the direct acting vasodilators (A: sodium nitroprusside [SNP 10 μg/kg i.v.] and B: adenosine [300 μg/kg i.v.]) in Lewis, Lewis polycystic kidney (LPK) and spontaneously hypertensive rats (SHR). Results are expressed as mean ± SEM. *P <0.05 compared to Lewis.
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fig03: Ratio of the mean arterial pressure (MAP) response after ganglionic blockade (hexamethonium 8 mg/kg i.v.) to that of the direct acting vasodilators (A: sodium nitroprusside [SNP 10 μg/kg i.v.] and B: adenosine [300 μg/kg i.v.]) in Lewis, Lewis polycystic kidney (LPK) and spontaneously hypertensive rats (SHR). Results are expressed as mean ± SEM. *P <0.05 compared to Lewis.

Mentions: The response to 8 mg/kg hexamethonium was used for normalization as it was the dose at which no further fall in either MAP or SBP was seen across all three strains. In Lewis control rats, the doses of SNP and adenosine that produced comparable reductions in MAP and SBP to 8 mg/kg hexamethonium were identified. For SNP, this was identified as 10 μg/kg for both MAP and SBP (MAP: hexamethonium 8 mg/kg −35 ± 4 vs. SNP 10 μg/kg −36 ± 1 mmHg; SBP: hexamethonium 8 mg/kg −52 ± 4 vs. SNP 10 μg/kg: −55 ± 2 mmHg, both P >0.05). For adenosine it was determined to be 300 μg/kg for both MAP and SBP (MAP: hexamethonium 8 mg/kg −35 ± 4 vs. adenosine 300 μg/kg −31 ± 2 mmHg; SBP: hexamethonium 8 mg/kg: −52 ± 4 vs. adenosine 300 μg/kg −45 ± 3 mmHg; both P >0.05). Consequently, the depressor responses to 10 μg/kg SNP and 300 μg/kg adenosine were used to normalize the response to ganglionic blockade (both MAP and SBP) in all three strains. The ratio of the reduction in MAP in response to administration of hexamethonium/SNP and hexamethonium/adenosine is illustrated in Fig. 3. In the LPK, both of these ratios were greater than that obtained in the Lewis controls. No difference in these ratios relative to the SHR was observed in the LPK. When these ratios were calculated using SBP (Fig. 4), both ratios were again greater in the LPK compared with Lewis and the adenosine response was also significantly greater than that of the SHR.


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)

Ratio of the mean arterial pressure (MAP) response after ganglionic blockade (hexamethonium 8 mg/kg i.v.) to that of the direct acting vasodilators (A: sodium nitroprusside [SNP 10 μg/kg i.v.] and B: adenosine [300 μg/kg i.v.]) in Lewis, Lewis polycystic kidney (LPK) and spontaneously hypertensive rats (SHR). Results are expressed as mean ± SEM. *P <0.05 compared to Lewis.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig03: Ratio of the mean arterial pressure (MAP) response after ganglionic blockade (hexamethonium 8 mg/kg i.v.) to that of the direct acting vasodilators (A: sodium nitroprusside [SNP 10 μg/kg i.v.] and B: adenosine [300 μg/kg i.v.]) in Lewis, Lewis polycystic kidney (LPK) and spontaneously hypertensive rats (SHR). Results are expressed as mean ± SEM. *P <0.05 compared to Lewis.
Mentions: The response to 8 mg/kg hexamethonium was used for normalization as it was the dose at which no further fall in either MAP or SBP was seen across all three strains. In Lewis control rats, the doses of SNP and adenosine that produced comparable reductions in MAP and SBP to 8 mg/kg hexamethonium were identified. For SNP, this was identified as 10 μg/kg for both MAP and SBP (MAP: hexamethonium 8 mg/kg −35 ± 4 vs. SNP 10 μg/kg −36 ± 1 mmHg; SBP: hexamethonium 8 mg/kg −52 ± 4 vs. SNP 10 μg/kg: −55 ± 2 mmHg, both P >0.05). For adenosine it was determined to be 300 μg/kg for both MAP and SBP (MAP: hexamethonium 8 mg/kg −35 ± 4 vs. adenosine 300 μg/kg −31 ± 2 mmHg; SBP: hexamethonium 8 mg/kg: −52 ± 4 vs. adenosine 300 μg/kg −45 ± 3 mmHg; both P >0.05). Consequently, the depressor responses to 10 μg/kg SNP and 300 μg/kg adenosine were used to normalize the response to ganglionic blockade (both MAP and SBP) in all three strains. The ratio of the reduction in MAP in response to administration of hexamethonium/SNP and hexamethonium/adenosine is illustrated in Fig. 3. In the LPK, both of these ratios were greater than that obtained in the Lewis controls. No difference in these ratios relative to the SHR was observed in the LPK. When these ratios were calculated using SBP (Fig. 4), both ratios were again greater in the LPK compared with Lewis and the adenosine response was also significantly greater than that of the SHR.

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