Cardiovascular Physiology Fall - The course with a heart!


Control of Arterial Blood Pressure and Blood Volume
Rev. 6/23/05


We have been examining the interactions of the short and long term pressure regulation systems. A classic experiment in the area of BP regulation is the one run originally by Goldblatt. All similar experiments since have also been called "Goldblatt" hypertension experiments.

In such an investigation, the renal arteries to one or more of the kidneys are clamped, reducing renal perfusion pressure (RENPP) and flow (RBF)This is achieved in web-HUMAN by adjusting the parameter CLAMP. The kidneys, "thinking" the problem is one of too low a systemic perfusion pressure (i.e. too low a blood pressure), react by trying to raise systemic blood pressure back towards normal by renin-induced volume regulation. This correction finally results, as long as the renal arteries remain clamped, in a near normal renal perfusion pressure bought at the price of a chronically raised systemic pressure. In the case of real (i.e. non-simulated) renal artery stenosis in a patient, caused by say renal arterial sclerosis, exactly the same series of events could result in that person having massive (systemic) hypertension.

One reason the results of such an experiment are interesting to us as students of cardiovascular physiology is because there are really two categories of events going on. One, as outlined above, are the attempts by the kidney to restore its own pressure and flow to normal and the resulting systemic hypertension. The second is a reaction by the cardiovascular control system to what is happening in the rest of the body, which it sees as too high a pressure and flow (i.e. a systemic hypertension). That is, from the viewpoint of all the other (i.e. non-renal) regulatory systems, what they see is hypertension and their response is an attempt to lower ststemic arterial pressure back towards normal.


Set the variable CLAMP to 40. This effects a clamp of the renal arteries bilaterally such that the pressure drops by 40 mmHg across the clamp resistance. Thus, an AP of 100 mmHg will result post-clamp in a renal perfusion pressure (RENPP) of 60 mmHg.

Follow both the short and long term response components by running the experiment for 1 day at 30 min. intervals (=short term) and then continuing for 16 days (16 D) at 1 day intervals between printouts (long term).

The response involves quite a few subsystems. I suggest that you repeat the experiment 4 times (each time starting over) reading out in your table headers the following "systems" and variables.

1) volume responses (Tables headers)


2) hemodynamic response


3) renal output/hormones


4) sympathetic response/renal variables



Print out the results of each of the four above experimental runs.

You should consult the on-line variables list in HUMAN to help you translate those six letter HUMAN variables mnemonics that you are still unfamiliar with into into their physiological equivalents.


Specific questions

1) PCOP (plasma colloid osmotic pressure, mmHg) generally drops during the response. Discuss why.


2) The SYMPNA (sympathetic nervous system activity, 1.00 is 'normal') decreases during day #1 as does PNOR (plasma norepinephrine, µ g/ ml blood, 0.200 is 'normal'). Why?


3) SVOL (stroke volume, ml, sympathetic data sheet) largely rises as does MCFP (mean circulatory filling pressure, mmHg, hemodynamics data sheet). Explain the cause of the change in each and the advantage of each change in controlling blood pressure.


General Analysis

1) Characterize the mechanisms active in the short term response by citing specific data patterns from web-HUMAN.

2) Characterize the mechanisms active in the long term response by citing specific data patterns from web-HUMAN.

3) Document from the data the 'attempts' of the baroreceptor system to oppose the renal response.