Respiratory sympathetic modulation is augmented in chronic kidney disease

Area of Science:

• Cardiovascular Physiology
• Renal Physiology
• Neuroscience

Background:

• Hypertension is a common complication of chronic kidney disease (CKD).
• The sympathetic nervous system plays a crucial role in regulating blood pressure.
• Respiratory modulation of sympathetic nerve activity (respSNA) is a physiological mechanism influencing cardiovascular control.

Purpose of the Study:

• To investigate respiratory modulation of sympathetic nerve activity in a rodent model of hypertension and CKD.
• To compare respSNA between hypertensive CKD rats (LPK) and control rats.
• To examine the effects of hypoxia and hypercapnia on respSNA in both strains.

Main Methods:

• In vivo recordings of splanchnic and renal nerve activity in anesthetized adult rats.
• Ex vivo working heart brainstem preparation to assess thoracic sympathetic nerve activity in juvenile rats.
• Application of peripheral (hypoxia, NaCN) and central (hypercapnia) chemoreceptor challenges.

Main Results:

• Amplified respSNA was observed in LPK rats compared to Lewis controls under basal conditions.
• Both hypoxia and hypercapnia increased respSNA in both strains, with a greater magnitude in LPK rats, especially during hypoxia.
• Peripheral chemoreceptor activation (NaCN) elicited a larger respSNA increase in LPK rats.

Conclusions:

• Amplified respiratory modulation of sympathetic nerve activity is a characteristic feature of this hypertensive CKD model.
• This amplified respSNA may be a contributing factor to the development and maintenance of hypertension in CKD.
• The findings highlight a potential mechanism linking CKD, sympathetic overactivity, and cardiovascular disease.