Table 4.
A possible approach to distinguishing among types of disorders associated with chronically increased renin secretion from kidneys
| Possible types of increased renin secretion | Renovascular or Goldblatt's hypertension | Diabetic nephropathy | “Psychogenic hypertension” | Comments | |
|---|---|---|---|---|---|
| The basic mechanism | Some nephrons are perfused under suboptimal pressure due to stenotic renal arteries | In all nephrons JGAs are activated due to increased sodium absorption in proximal tubules caused by glucose overload | Sympathetic stimulation of β1 receptors activates JGA in many nephrons | Renovascular hypertension is unique in its regional nature, the hypoperfused kidney alters arterial pressure, systemic resistance and kidney performance | |
| Kidney perfusion | normal or modestly decreased | increased | slightly decreased | Diabetic nephropathy forces both kidneys to supranormal perfusion and filtration, diuresis often relieves hypertension. ACE inhibitors or AT1R blockers can normalize filtration, but perfusion usually remains increased | |
| Kidney filtration rate | normal or modestly decreased | increased | normal | ||
| Arterial hypertension | always | in some cases | always | ||
| Systemic vascular resistance | increased | increased | increased | ||
| RAS components | Medication | Effects of medication on plasma levels of RAS components | |||
| high renin | ACE inhibitors | no reduction | no reduction | no reduction | Pressure normalization in all three types due to the reduced exposure of AT1R receptors in arterioles to the circulating Ang II |
| high Ang I | ACE inhibitors | no reduction | no reduction | no reduction | |
| high Ang II | ACE inhibitors | decreased AT II production by ACE | decreased AT II production by ACE | decreased AT II production by ACE | |
| high renin | AT1R blockers | no reduction | no reduction | no reduction |
Pressure normalization in all three types due to the blocked AT1R activation. Increased availability of AT II allows more interactions with AT2R and other receptors |
| high Ang I | AT1R blockers | no reduction | no reduction | no reduction | |
| high Ang II | AT1R blockers | no reduction | no reduction | no reduction | |
| high renin | Nebivolol | no reduction | no reduction | reduced | Pressure normalization by blocking β1 receptors only in the “psychogenic hypertension” |
| high Ang I | Nebivolol | no reduction | no reduction | reduced | |
| high Ang II | Nebivolol | no reduction | no reduction | reduced | |
Renovascular hypertension and Diabetic nephropathy are based on refs 4, 5, 6, 7, the proposed “Psychogenic hypertension” on refs 42, 56 and 57. Changes in plasma levels of renin, Ang I and Ang II, before and after the introduction of nebivolol might help in detection of patients with “Psychogenic hypertension”, due to an increased allostatic load.