From the Guidelines
Afferent arteriolar vasodilation is primarily caused by prostaglandins, nitric oxide, and dopamine, while vasoconstriction is mediated by angiotensin II, thromboxane A2, endothelin, adenosine, and sympathetic nervous system activation through norepinephrine, as evidenced by the complex interplay of these substances in renal physiology 1.
Key Regulators of Afferent Arteriolar Tone
In the context of glomerulotubular feedback, several key chemicals and hormones regulate afferent arteriolar tone, including:
- Prostaglandins (particularly PGE2 and PGI2)
- Nitric oxide (NO)
- Dopamine, which are vasodilators that increase renal blood flow and glomerular filtration rate by relaxing the smooth muscle of the afferent arteriole
- Angiotensin II, which is a potent vasoconstrictor that plays a crucial role in the renin-angiotensin-aldosterone system
- Thromboxane A2
- Endothelin
- Adenosine
- Sympathetic nervous system activation through norepinephrine, which mediate afferent arteriolar vasoconstriction
Mechanism of Glomerulotubular Feedback
The macula densa cells in the distal tubule sense sodium chloride concentration and signal for appropriate vascular adjustments, with high sodium concentrations typically triggering vasoconstriction and low concentrations promoting vasodilation, as described in the context of renal considerations in angiotensin converting enzyme inhibitor therapy 1. This feedback mechanism helps maintain homeostasis in kidney function and systemic blood pressure regulation.
Clinical Implications
Understanding the regulators of afferent arteriolar tone is essential for managing conditions that affect renal function, such as hypertension and chronic kidney disease, where the balance between vasodilatory and vasoconstrictive influences plays a critical role in maintaining appropriate glomerular filtration rates, as highlighted in the study on renal considerations in angiotensin converting enzyme inhibitor therapy 1.
From the Research
Chemicals and Hormones Involved in Afferent Arteriolar Vasodilation and Vasoconstriction
- Adenosine: plays a role in mediating efferent arteriole vasodilation in response to increased NaCl concentration at the macula densa, acting through its A2 receptor 2
- Nitric oxide (NO): derived from neuronal NO synthase (nNOS) in the macula densa, regulates afferent arteriolar diameter 3
- Sodium chloride (NaCl): high concentrations in the tubular fluid stimulate the macula densa to initiate a cascade of events resulting in efferent arteriole vasodilation 2 and afferent arteriole vasoconstriction through tubuloglomerular feedback (TGF) 4, 5
- Epithelial sodium channel (ENaC): mediates connecting tubuloglomerular feedback (CTGF) and contributes to the regulation of renal blood flow and glomerular filtration 4, 5, 6
Mechanisms of Afferent Arteriolar Vasodilation and Vasoconstriction
- Tubuloglomerular feedback (TGF): a vasoconstrictor mechanism initiated in the macula densa via Na-K-2Cl cotransporters (NKCC2) 5
- Connecting tubuloglomerular feedback (CTGF): a vasodilator mechanism initiated in connecting tubules via epithelial sodium channels (ENaC) 4, 5, 6
- Luminal flow in the connecting tubule: induces afferent arteriole vasodilation through CTGF, partially due to flow-stimulated O2- production 6