Internephron coupling by conducted vasomotor responses in normotensive and spontaneously hypertensive rats

Abstract

We compared conducted vasomotor responses in juxtamedullary microcirculation in normotensive Sprague-Dawley (SD) and spontaneously hypertensive rats (SHR). The goals of the study were as follows: 1) decide whether internephron coupling is facilitated by conducted vasomotor responses; 2) determine whether the magnitude of induced vasoconstriction decreases with increasing distance from the stimulation site; and 3) determine whether the response is stronger in SHR than in SD rats. Microapplication of KCl to the distal afferent arteriole caused local vasoconstriction that was rapidly conducted (speed > 3.0 mm/s) into the cortical radial artery and neighboring afferent arterioles in SD and SHR. The strength of the response was significantly greater (approximately 40%, P < 0.025) in SHR than SD, and the magnitude decreased monotonically with increasing distance from the stimulation site in both strains. Mechanical length constants were similar in SD and SHR (approximately 325 microm), indicating that the signal responsible for the effect decays at the same rate in both strains. We conclude that internephron coupling strength is significantly greater in SHR and that internephron coupling is due to vascular events conducted along the preglomerular vasculature.

Vascular coupling induces synchronization, quasiperiodicity, and chaos in a nephron tree

“…The signals are initiated by TGF, the mechanism that provides local regulation of blood flow, and influences the vascular response of adjacent nephrons. 4,6,21,22 We used the simulation to address several questions. First, is nephron-to-nephron communication sufficient to explain the strong synchronization of tubular pressure oscillations found in normal rats and those with hypertension.…”

“…Equation ͑2͒ expresses the current state of knowledge of the interaction; a change in the TGF signal in one nephron can be detected in the TGF mechanism of a neighboring nephron, and the effect of the interaction decreases exponentially with the vascular distance the signal must traverse. 6,21,22 The mechanisms underlying these interactions are presently not known in detail and we offer no hypothesis regarding them.…”

“…21,22 The renal cortex is about 2 mm deep in rats, and the cortical radial artery branches from the arcuate artery and penetrates toward the renal surface within the cortex. We assume, therefore, that the field of interacting nephrons consists of all those with afferent arterioles originating from a single cortical radial artery, which includes superficial ͑cortical͒ as well as deep ͑juxtamedullary͒ nephrons.…”

“…The value of this parameter is in the range 0.25-0.5 in normal animals. 21,22 As mentioned above, oscillations in tubular pressure are typically measured in normal rats over the arterial pressure range 95-130 mm Hg. Figure 7͑a͒ shows a region of chaotic behavior in the arterial pressure range 100-115 mm Hg when lies between 0.25 and 0.5.…”

Sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up

“…Based on the viability tests performed and the observation of conduction of other stimuli in our set‐up, we do not believe that the vessels might have been damaged, disrupting the cell‐cell communication. Conduction of responses to local K + has been observed in hamster cheek pouch and rat kidney arterioles,35, 36 as well as in mesenteric arterioles 37. In this latter case, terminal arterioles were used (fifth order branch).…”