Thank you for the question - and sorry I have been tardy, but I have been unwell.
Yes, frusemide (Furosemide) is a venodilator, along with a number of other agents ... especially the short-acting nitrates like GTN, and the longer acting nitrates like isosorbide mononitrate ... and act to dilate (enlarge) the great veins and thus increase their capacity to hold blood (venous capacitance). This reduces the so-called pre-load ... the rate of blood returning to the right side of the heart ... and thus, venodilators are especially useful in the early treatment of acute states like pulmonary oedema.
When given in the EMD for acute pulmonary oedema, the first (and arguably most telling) action of frusemide is NOT as a diuretic - that benefit comes much later in time - but as a venodilator ... expanding the ‘holding capacity’ of the great veins, and thereby (albeit briefly) reducing the rush of venous blood back into the right side of the heart, and in turn, thus lessening the flood of venous blood on and into the pulmonary circulation. This ‘buys time’ for the struggling left heart (esp. the left ventricle) to begin to ‘play catch-up’, and pump blood on and out of the lungs and into the systemis circulation. As the failing left heart begins to ‘win’ - having been given precious minutes of ‘breathing’ space (pun intended) by the sudden venodilator (frusemide + nitrate) driven reduction in pre-load - the lungs begin to be emptied of excess blood and fluid. This then leads to better oxygenation of blood in the improving lungs, which in turn improves left heart function. The gasping patient visibly begins to breathe more easily as the lungs begin to dry out. As left heart function improves, cardiac output improves. This benefits renal perfusion. Finally, over the subsequent few hours, frusemide begins to stimulate a diuresis. But, the super-key action of frusemide - in this context ... along with the nitrate absorbed from the always applied nitrate patch ... is the pre-load reduction achieved through venodilatation in those first few minutes. The frusemide-driven diuresis that follows in the hours later, while important overall, is not the lifesaving thing. What saves life is the pre-load reduction - and that is a seconds and minutes thing!
So ...frusemide works in acute pulmonary oedema - at least in part as a venodilator ... and this will still be the case, even in anuric states, when its 'main action' as a diuretic is clearly no longer going to play a later role.
However, as an adjunct to the treatment of systemic hypertension in anuria ... the nub of your question ... that’s a different situation. And, no ... I doubt it would be of much (or any) use as an effective systemic anti-hypertensive agent in anuric states.
But ... the medical word ‘hypertension’ isn’t quite as simple as it seems. It covers far wider ground than just ‘the blood pressure’. Let me try to explain ...
There are 3 or 4 main applications of the word ‘hypertension’ ... but most only understand - or think - that there is only one.
Everyone knows of (1) the systemic hypertension ... the blood pressure (xxx over xx) as a reflection of the systolic pressure over the diastolic pressure. But, there ARE 2 OTHER distinct and separate vascular ‘beds’ (and a 3rd - though it is more a ‘cavity ... the intracranial cavity inside the rigid skull), all with their own versions of ‘hypertension’. Each can lay its own claim to the word ‘hypertension’. After all, ‘hypertension’ simply means an elevated pressure but it doesn’t stipulate where, I do not intend to further pursue intracranial hypertension further, here.
The 2 other main ‘vascular’ sorts of hypertension are (2) pulmonary hypertension (see the following discussion) ... and (3) glomerular hypertension, a vastly and vitally important concept entirely within the kidney itself ... but I will not discuss glomerular hypertension further in this answer.
Germane to your question about frusemide, blood pressure and anuria, read on.strong text
Your question mentioned ‘hypertension’ ... but referrals to frusemide, which? systemise or Pulmonary HT?’
If your question had referred to pulmonary hypertension, then the answer is ‘yes’, there certainly IS a role for venodialtors there! That made me wonder if you may have confused systemic hypertension (which is suggested by the inclusion of 'difficult to control BP' in your question) with pulmonary hypertension = an elevation in pulmonary artery pressure. So ... let me dwell on pulmonmary hypertension = quite commonly a factor .. and that sometimes poses a severe and difficult treatment problem .. in some patients on dialysis.
Importantly ... systemic hypertension and pulmonary hypertension are not at all the same.
Systemic hypertension describes an elevated pressures on the output side of the heart ... the left heart ... and is associated with an elevation in blood pressure. This is the sort of ‘hypertension’ that most people mean and think of when they use the word 'hypertension'.
Here, the standard treatments include salt restriction, a raft of differently working medications that broadly fall into the categories of beta blockers (the '-olols'), ACE inhibitors (the '-prils), angiotensin receptor blockers (the '-sartans'), calcium channel blockers (the '-zems' and the '-ipines'), the vasodilators (a mixed group including prazosin and minoxidil), and the centrally acting agents (like methyl dopa, clonidine, and moxonidine) ... and the diuretics (of which frusemide is one, along with the thiazides, and others). Here, the diuretics cant offer much, unless there is a urine output to work with, so 'anuria' in your question essentially precludes value for diuretics as an effective BP medication.
Pulmonary hypertension, on the other hand, affects the capacity of the right heart to on-circulate returning venous blood into the pulmonary circulation (the lungs) for re-oxygenation. It is the pressure within the pulmonary circulation (the lungs) and is a measure of pulmonary artery pressure, and NOT the systemis pressure.
The treatment of pulmonary hypertension is a very different kettle of fish! This is a very specialised area of cardiac and circulatory management using a range of much more complex agents - including some of the protaglandin agents, the nitrates, diuretics etc. But, in an anuric person, that complexity reaches another level again and becomes even more challenging.
So ... in summary, and while I may be wrong in my suspicion that you may have confused systemic with pulmonary hypertension, then as regards the usefulness of frusemide in the treatment of 'hypertension', I would say
'YES' in systemic hypertension with a urine output ... but
‘NO' in systemic hypertension without a urine output ... while I would say
'YES' to its use in chronic pulmonary hypertension both with or without a urine output, although there are other agents in chronic pulmonary hypertension likely to give a much bigger bang for the buck.
As for the use of frusemide in acute pulmonary hypertension (as occurs in acute pulmonary oedema), the use of frusemide is a definite 'YES' - even a MUST' - whether or not there is a urine output.
Finally, there remains the issue of the use of (often high dose) frusemide in dialysis patients to sustain a residual urine output from the background, failing, native kidneys - if only to help benefit oral fluid freedom. That, too, is a different story,. It has proponents - either way - and is not something to get into here. I rather fancy I have discussed this before in these message board answers ... so ... have a search using the search function, if you want to explore this aspect further.